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154 Cards in this Set
- Front
- Back
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tidal volume
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volume inspired or expired with each normal breath
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inspiratory reserve volume
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-volume that can be inspired over and above tidal volume
-used during exercise |
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expiratory reserve volume
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volume that can be expired after expiration of a tidal volume
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residual volume
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-cannot be measured by spirometry
-volume that remains in lungs after maximal expiration |
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dead space (anatomic)
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volume of conducting airways (150 mL)
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dead space (physiologic)
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-functional measurement
-volume of lungs that does not participate in gas exchange -appx equal to anatomic dead space in normal lungs - can be greater in lung diseases in which there are ventilation/perfusion (V/Q) defects |
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formula for physiologic dead space
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VD= VT x [(PaCO2-PeCO2)/(PaCO2)]
VD- physiological dead space VT- tidal volume PaCO2- PCO2 of alveolar gase=PCO2 of arterial blood PeCO2- PCO2 of expired air |
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what does the equation actually mean
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physiologic dead space is tidal volume multiplied by a fraction
- fraction is dilution of alveolar PCO2 by dead-space air- does not participate in gas exchange and does not contribute CO2 to expired air |
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minute ventilation
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tidal volume x breaths/min
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alveolar ventilation
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(tidal volume-dead space) x breaths/min
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inspiratory capacity
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sum of tidal volume and IRV
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functional residual capacity
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sum of ERV and residual volume
- volume remaining in lungs after a tidal volume is expired - includes residual volume so cannot be measured |
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vital capacity- forced vital capacity
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sum of tidal volume, IRV, and ERV
- volume that can be forcibly expired after a maximal inspiration |
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total lung capacity (TLC)
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sum of all four lung volumes
- volume in lungs after a maximal inspiration - includes residual volume so cannot be measured by spirometry |
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FEV1
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-forced expiratory volume
- volume of air that can be expired in the first second of a forced maximal expiration - normally 80% of forced vital capacity (FEV1/FVC= 0..8) |
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obstructive lung disease effect on FEV1
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FEV1 reduced more than FVC so ratio decreased
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restrictive lung disease effect on FEV1
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both FEV1 and FVC are reduced and ratio is normal or increased
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compliance
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C=V/P
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compliance characteristic
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- describes the distensibility of the lungs and chest wall
- inversely related to elastance, which depends on amount of elastic tissue - inversely related to stiffness - slope of pressure-volume curve - change in volume for a given pressure |
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transmural pressure
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alveolar pressure- intrapleural pressure
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what happens to lung when pressure outside the lungs (transpleural) is negative
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lung expands- lung volume increase
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what happens when pressure outside lungs (intrapleural pressure) is positive
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lungs collapse and volume decreases
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difference between inflation and deflation curve of lung
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hysteresis
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when is compliance greatest
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in the middle range of pressures- lungs are most distensible
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compliance of the lung-chest wall system compared to lungs alone or chest wall alone
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compliance is less- slope is flatter
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at rest- lung volume is at FRC and pressure in airways and lungs is equal to atmospheric pressure (0)- what kind of force on lungs and chest wall
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collapsing force on lungs and expanding force on chest wall
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at FRC why does the combined lung-chest wall system neither collapsing or expanding
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the two forces are equal and opposite
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at FRC with both opposin forces, what is intrapleural pressure
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negative (subatmospheric)
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if air is introduced to intrapleural space (pneumothorax), what happens to intrapleural pressure
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becomes equal to atmospheric pressure
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with pneumothorax what happens to lungs and chest wall
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lungs will collapse (natural tendency)
chest wall will spring out (natural tendency) |
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change in lung compliance with emphysema
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compliance is increased- tendency of lungs to collapse is decreased
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why does a patient's chest become barrel-shaped in emphysema
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system seeks higher FRC so that two opposing forces can be balanced- higher volume
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change in lung compliance with fibrosis
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lung compliance is decreased- tendency to collage is increased
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alveolar surface tension result of
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-attractive forces between liquid molecules lining alveoli
- creates a collapsing pressure that is directly proportional to surface tension and inversely proportional to alveolar radius (Laplace's Law) |
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LaPlace's Law formula
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P= 2T/r
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collapsing pressure in large alveoli
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low collapsing pressures and are easy to keep open
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collapsing pressure in small alveoli
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high collapsing pressures and are more difficult to keep open
- absence of surfactant- small alveoli tend to collapse- atelectasis |
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surfactant characteristics
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- lines alveoli
- reduces surface tension--> prevents collapse and increases compliance - made by type II alveolar cells - made mostly of dipalmitoyl phosphatidylcholine |
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when is surfactant present in the fetus
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as early as week 24 and almost always present by week 35
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level of lecithin: sphingomyelin ratio indicating mature levels of surfactant
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2:1
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neonatal RDS
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premature infants because lack surfactant
- infant shows atelectasis (lungs collapse); difficulty reinflating lungs (decreased compliance); hypoxemia (decreased V/Q) |
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what is airflow driven by and directly proportional to
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pressure difference between mouth and alveoli
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what is airflow inversely proportional to
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airway resistance- Q= changeP/R
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Pouiseuille's law
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R= 8nl/pir2
-resistance= inversely proportion to the radius to the 4th power - directly proportional to the viscosity and length of inspired gas |
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major site of airway resistance
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medium-sized bronchi
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parasympathetic result on bronchial smooth muscle
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constricts airways, decreases radius, increases resistance
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two other substances that constrict airways
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irritants, slow reacting substance of anaphylaxis (asthma)
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sympathetic stimulation result on bronchial smooth muscle (and sympathomimetics- isoproterenol)
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dilate airways via B2 receptors- increase radius, decrease resistance
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high lung volumes are associated with what
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greater traction exerted on airways and decreased resistance- pts breath at higher lung volumes to offset high airway resistance of dx
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low lung volumes are assd with what
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low traction on airways around tissue and increased airway resistance- bad sometimes
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pressure findings at rest before inspiration
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avleolar pressure= atmospheric pressure
- alveolar pressure is said to be 0 |
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intrapleural pressure at rest before inspiration
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negative- opposing forces trying to collapse and chest wall tryin to expand creating negative pressure in intrapleural space between them
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what happens in inspiration
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- inspiratory muscle contract
- volume of thorax increases - as lung volume increases, alveolar pressure decreases to subatmospheric - airflow will continue until pressure gradient dissipates |
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intrapleural pressure during inspiration
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becomes more negative because lung volume increases, elastic recoil strength also increases
- even more negative than it was at rest |
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at peak of inspiration what is calculation for lung volume
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FRC + TV
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what happens in expiration
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- alveolar pressure becomes greater than atmospheric pressure because alveolar gas is compressed by elastic forces of the lung
- alveolar pressure is higher that atm pressure- gradient reverse- air flows out |
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intrapleural pressure during normal expiration
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returns to resting state
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intrapleural pressure during forced expiration
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becomes positive and compresses airways- makes expiration hard
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COPD
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airway resistance is increased; patients expire slowly w pursed lips to prevent airway collapse that could occur w forced expiration
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asthma
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-obstructive disease where expiration is impaired
- characterized by decreased FVC, decreased FEV1, and DECREASED ratio - air that should have is not expired--> air trapping and increased FRC |
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COPD
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-combo of bronchitis and emphysema
- increased lung compliance and expiration is empaired - decreased ratio FEV1/FVC - increased FRC, air trapping, barrel chest |
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pink puffers
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emphysema
- mild hypoxemia but maintain alveolar ventilation so normocapnic |
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blue bloaters
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bronchitis
- severe hypoxemia with cyanosis- do not maintan alveolar ventilation- hypercapnic |
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complications of bronchitis
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R ventricular failure; systemic edema
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fibrosis
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restrictive disease with decreased lung compliance- inspiration impaired
- decrease in all lung volumes- ratio normal or increased |
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dalton's law of partial pressures
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partial pressure= total pressure x fractional gas concentration
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partial pressure of O2 in dry inspired air
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PO2= 760 mmHg x 0.21= 160 mmHg
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partial pressure of O2 in humidified tracheal air
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Ptotal= 760mmHg- 47 mmHg (PH20)= 713mmHg
PO2= 713mmHg x 0.21= 150 mmHg |
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what percent of systemic CO bypasses pulmonary circulation
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2%- physiologic shunt- resulting admixture makes PO2 of arterial blood slightly lower than that of alveolar air
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amount of gas dissolved in a solution is proportinoal to what
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partial pressure
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* partial pressures of O2 in dry inspired air, humidified tracheal air, alveolar air, systemic arterial blood, and mixed venous blood
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160 mmHg, 150 mmHg, 100mmHg, 100mmHg (blood equilibrates w alveolar air), 40mmHg
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*partial pressures of CO2 in dry air, humidified tracheal air, alveolar air, systemic arterial blood, and mixed venous blood
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0mmHg, 0mmHg, 40mmHg, 40mmHg, 46mmHg
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what do diffusion rates of O2 and CO2 depend on
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partial pressure differences across membrane and surface area
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perfusion-limited exchange
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gas equilibrates early along the length of pulm capillary
- diffusion of the case ban be increased only if blood flow increases |
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diffusion-limited exchange
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- CO and O2 during exercise
- fibrosis |
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diffusion-limited exchange in fibrosis
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diffusion of O2 is restricted because thickening of alveolar membrane increases diffusion distance
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diffusion-limited exchange in emphysema
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diffusion of O2 is decreased because surface area for diffusion is decreased
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oxygen transport
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dissolved or bound to hemoglobin
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hemoglobin make up
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-4 subunits
- each contains a heme moiety- iron-containing porphyrin - iron is in Fe2+ (ferrous) state and binds O2 - each subunit- a polypeptide chain - two have a chains; two have B chains (normal adult: a2B2) |
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fetal hemoglobin
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B chains replaced by y chains
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affinity of fetal hemoglobin for oxygen vs adult
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O2 affinity higher in fetal (left shift) because 2,3-diphosphoglycerage binds less avidly
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what benefit is it for fetal Hgb to have a higher affinity for O2
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O2 movement from mother to fetus is facilitated
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O2 binding capacity of blood
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maximum amt of O2 that can be bound to Hgb
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O2-binding capacity of blood depends on
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Hgb concentration in blood- limits amount of O2 that can be carried in blood; measured at 100% saturation
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O2 content of blood
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total amount of O2 carried in blood, including bound and dissolved
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O2 content of blood depends on
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Hgb concentration, PO2, and P50 of Hgb
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equation for O2 content of blood
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O2 content= (O2 binding capacity x % saturation) + dissolved O2
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hemoglobin state in arterial blood at PO2 of 100 mmHg
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100% saturated; O2 is bound to all 4 heme groups
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hemoglobin state in mixed venous blood at PO2 of 40 mmHg
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hemoglobin is 75% saturated; on average, 3/4 heme groups have attached O2
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hemoglobin state at a PO2 of 25mmHg
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hemoglobin is 50% saturated, 2/4 heme groups have O2 bound
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shape of hemogloin-O2 dissociation curve when PO2 is between 60mmHg and 100mmHg
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almost flat- humans can tolerate changes in atmospheric pressure without compromising O2-carrying capacity of Hgb
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shifts to the right indicates what
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affinity of hemoglobin for O2 is decreased
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causes of shifts to the R
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- increased PCO2/ decreased pH
- increased temperature - increased 2,3-DPG: bind to B chains of deoxyhemoglobin and facilitate unloading of O2 |
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shifts to the left indicate what
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affinity of hemoglobin for O2 is increased
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causes of shifts to the L
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- decreased PCO2
- increased pH - decreased temp - decreased 2,3-DPH |
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what does CO poisoning do to the curve
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-CO competes with O2 for binding on hemoglobin
- affinity for CO is 200x that for O2 - CO takes binding sites- decreases O2 content of blood - increases affinity of other binding sites for O2- causes shift to L |
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hypoxemia
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- decrease in arterial PO2
- A-a gradient used to compare causes |
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alveolar PO2 calculation via alveolar gas equation
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PAO2= (PiO2-PACO2)/ R
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normal A-a gradient
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< 10mmHg- normally close because they equilibrate
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causes of A-a gradient to be >10
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if O2 does not equilibrate between alveoli and arterial
- diffusion defect, V/Q defect, R-to-L shunt |
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hypoxia
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decreased O2 delivery to the tissues
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equation for O2 delivery
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O2 delivery= C.O. x O2 content of blood
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what can cause hypoxia
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decreased C.O., decreased O2-binding capacity, decreased arterial PO2
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forms of CO2 in blood
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1.) dissolved CO2- small amt in free solution
2.) carbaminohemoglobin- small amt- CO2 bound to hemoglobin 3.) HCO3- is 90% |
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carbonic anyhydrase catalyzes what reaction
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CO2 + H2O--> H2CO3 which dissociates to H+ and HCO3-
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chloride shift
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HCO3- leaves RBC in exchange for Cl-
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H+ buffered inside the RBC how
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by deoxyhemoglobin
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pulmonary circulation- pressure
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pressures are much lower than in systemic circulation
- pulmonary arterial pressure is 15 mmHg (aorta=100mmHg) |
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pulmonary circulation- resistance
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much lower in pulmonary circulation
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cardiac output of R ventricle
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-pulmonary blood flow
- equal to cardiac output of L ventricle - it's cool though because even though pressure is low, resistance is also low so it is sufficient |
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what is the V/Q ratio when tidal volume, frequency, and C.O. are normal
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0.8
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normal V/Q ratio results in what values of arterial PO2 and arterial PCO2
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PO2- 100mmHg
PCO2- 40mmHg |
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both ventilation and perfusion are nonuniformly distributed in what lung
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normal upright lung
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where is blood flow lowest and highest
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lowest at the apex and highest at the base
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where is ventilation lowest and highest
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lowest at the apex and highest at the base; regional differences are not as significant as for perfusion
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V/Q ratio is higher where
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apex than base
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regional differences for PO2 as a result of V/Q ratio
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PO2 is highest at the apex and PCO2 is lower because there is more gas exchange
- PO2 is lowest and PCO2 is higher at the base because there is less gas exchange |
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what happens to V/Q ratio in airway obstruction
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- airway completely blocked- ventilation is zero
- blood flow normal- V/Q is 0 and called a shunt |
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what happens to values of PCO2 and PO2 in pulmonary capillary blood in a lung that is perfused but not ventilated
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- zero gas exchange
- will approach values in mixed venous blood - increased A-a gradient |
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V/Q ratio in pulmonary embolism
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- blood flow 0
- ventilation can be normal; so V/Q is infinate--> dead space |
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central control of breathing
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brain stem and cerebral cortex
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medullary respiratory center
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-in the reticular formation
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responsibility of dorsal respiratory group
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inspiration and generating basic rhythm for breathing
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input to the dorsal respiratory group
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vagus and glosopharyngeal nerves
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vagus nerve relays information from
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peripheral chemoreceptors and mecahnoreceptors in the lung
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glossopharyngeal nerve relays information from
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peripheral chemoreceptors
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output from the respiratory group travels to
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with phrenic nerve to diaphragm
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responsibility of ventral respiratory group
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- expiration
- not active during normal, quiet breathing - activated during exercise, when it is more active |
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apneustic center
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-lower pons
-produces deep and prolonged inspiratory gasp (apneusis) |
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pneumotaxic center
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- upper pons
- inhibits inspiration- regulates inspiratory volume and RR |
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medullary central chemoreceptors
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- sensitive to pH of CSF
- decreases in pH of CSF cause increases in breathing rate |
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how do these chemoreceptors sense PCO2 changes
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- CO2 diffuses easily
- lipid soluble so can cross BBB - CO2 combines with H20 to produce H2CO3 then splits to H+ and HCO3 - *H+ directly acts on chemoreceptors |
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locatino of carotid bodies
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bifurcation of common carotid arteries
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location of aortic bodies
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above and below the aortic arch
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decreases in arterial PO2 have what effect
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stimulate peripheral chemoreceptors and increase breathing rate
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what is the threshold for stimulation of peripheral chemoreceptors to increase breathing rate
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<60mmHg
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increases in arterial PCO2 have what effect
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stimulate peripheral chemoreceptors and increase breathing rate
- potentiate stimulation of breathing from hypoxemia - response of peripherals to CO2 is less important than response of centrals to CO2 |
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increase in arterial [H+] have what effect
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stimulate carotid body peripheral chemoreceptors directly, independent of changes in PCO2
- in metabolic acidosis, breathing rate is increased |
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lung stretch receptors- location and function
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-smooth muscle of airways
- when receptors are stimulated by distention of the lungs- produce a reflex decrease in breathing frequency (Hering-Breuer reflex) |
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irritant receptors- location and function
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- between airway epithelial cells
- stimulated by noxious substances |
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juxtacapillary receptors- location and function
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- alveolar walls, close to the capillaries
- engorgement of the pulmonary capillaries- left heart failure- stimulates J receptors- cause rapid, shallow breathing |
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joint and muscle receptors- activation and function
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- activated during movements of the limbs
- involved in the early stimulation of breathing during exercise |
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overview of what happens during exercise
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increase in ventilatory rate- matches increase in O2 consumption and CO2 production by body
- joint muscle receptors are activated during movement and cause increased breathing at onset of exercise |
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mean values for arterial PO2 and PCO2 vary how during exercise
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do not change
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pH changes during moderate exercise
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no change in arterial pH
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pH changes during strenuous exercise
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- pH decreases due to lactic acidosis
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changes in venous PCO2 during exercise and why
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- increases because excess CO2 produced by exercising muscle is carried to the lungs in venous blood
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pulmonary blood flow during exercise
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- increases because C.O. increases during exercise
- more pulmonary capillaries are perfused and more gas exchange occurs |
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distribution of V/Q ratios through the lung during exercise
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more even during exercise than at rest- resulting decrease in physiologic dead space
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high altitude effect on alveolar PO2
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decreased because barometric pressure is decreased
- arterial PO2 is also decreased- hypoxemia |
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result of hypoxemia on peripheral chemoreceptors
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stimulates them to increase ventilation rate
- this hyperventilation produces respiratory alkalosis- treated by ACETAZOLAMIDE |
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effect of hypoxemia on kidney
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stimulates production of EPO- increases production of RBCs- increased Hgb concentration, increased O2 carrying capacity of blood, increased O2 content of blood
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2,3-DPG concentrations in hypoxemia?
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increased, shifts curve to R- results in decreased affinity of Hgb for O2 and facilitates unloading
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pulmonic vascular response to hypoxemia
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pulmonary vascoconstriction- increase in pulmonary arterial pressure, increased work on R side of heart against higher resistance, hypertrophy of R ventricle
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