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180 Cards in this Set
- Front
- Back
What is the tidal volume?
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The volume inspired or expired during normal breathing
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What is the inspiratory reserve volume?
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The volume that can be inspired beyond the tidal volume
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What is the expiratory reserve volume?
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The volume that can be expired after expiration of the tidal volume
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What is the residual volume?
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The volume that remains in the lungs after a maximal expiration
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Can residual volume be measured by spirometry?
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No
|
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What is anatomic dead space?
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The volume of the conducting airways, because they do not participate in gas exchange
Approximately 150 ml (or about 1 ml/lb of body weight) |
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What is physiologic dead space?
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It is the total dead space (the volume of the lungs that doesn't participate in gas exchange)
In normal lungs, physiologic dead space is approximately equal to anatomic dead space, but when there are V/Q defects, it is greater than anatomic dead space |
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Formula for physiologic dead space
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Vd = Vt x [(PCO2 - PexpiredCO2) / PCO2]
Vt = tidal volume Note that PCO2 is arterial/alveolar |
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Formula for minute ventilation
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Minute ventilation = tidal volume x (breaths/min)
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Formula for alveolar ventilation
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Alveolar ventilation = (tidal volume - dead space) x (breaths/min)
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What is the inspiratory capacity?
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Tidal volume + IRV
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What is the functional residual capacity?
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ERV + RV
The volume remaining in the lungs after a tidal volume is expired |
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Can FRC be measured by spirometry?
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No, because it includes the residual volume
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What is the vital capacity?
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Also known as the forced vital capacity (FVC)
TV + IRV + ERV This is the volume of air that can be forcibly expired after a maximal inspiration (total lung capacity except for the RV) |
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What is the total lung capacity?
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The sum of all lung volumes; the volume in the lungs after a maximal inspiration
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Can TLC be measured by spirometry?
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No, because it includes RV
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Can VC be measured by spirometry?
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Yes
|
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What is the forced expiratory volume?
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Abbreviated as FEV1
This is the volume of air that can be expired in the first second of a forced maximal expiration |
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What is the normal value for FEV1/FVC?
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0.8 (80%)
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What happens to FEV1/FVC in obstructive lung disease?
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It decreases
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What happens to FEV1/FVC in restrictive lung disease?
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Normal or increased
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Is asthma an example of obstructive or restrictive lung disease?
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Obstructive
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Is fibrosis an example of obstructive or restrictive lung disease?
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Restricted
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What are the muscles that participate in inspiration?
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Diaphragm
External intercostals and accessory muscles -- only used during exercise and respiratory distress |
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What is the role of the diaphragm in inspiration?
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The most important inspiratory muscle
When the diaphragm contracts, the abdominal contents move downward and the ribs move upward and outward This increases the volume of the thoracic cavity |
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Is normal quiet expiration active or passive?
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Passive
Results from the elastic recoil of the inspiratory muscles |
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What are the expiratory muscles?
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Abdominal muscles -- compress the abdominal cavity and push the diaphragm upward
Internal intercostals -- pull the ribs down Note that these muscles only participate during exercise or when airway resistance is increased due to lung disease |
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What is respiratory compliance?
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Describes the distensibility of the lungs and chest wall
It is inversely related to elasticity (that is, as elasticity increases, compliance decreases) Inversely related to stiffness Compliance is the change in volume or a given change in pressure. The higher the compliance, the greater the change in volume for that pressure value |
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Formula for respiratory compliance
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C = V/P
V = volume P = transmural pressure |
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What is the transmural pressure?
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Alveolar pressure - intrapleural pressure
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What is intrapleural pressure?
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The pressure outside of the lungs, inside the thoracic cavity
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How does intrapleural pressure determine lung inflation and deflation?
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When the IPP is negative, the lungs expand, causing lung volume to increase
When the IPP is positive, the lungs collapse and lung volume decreases |
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What is hysteresis?
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When the volume-pressure relationship of the lungs is different for inspiration and expiration
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At what pressures is compliance the greatest?
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Middle range of pressures
High compliance = greatest distensibility At high pressures, compliance is low and the lungs are only slightly distensible |
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How does the compliance of the chest-wall system compare to the compliance of the lungs or chest wall along?
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It is greater
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Describe the state of pressure and lung volume at rest
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Lung volume is at FRC
Pressure in the airways and lungs is equal to atmospheric pressure (0 mmHg) There is a collapsing force on the lungs and an expanding force on the chest wall These forces are equal and opposite, so the chest-wall system does not collapse or expand These two opposing forces generate negative intrapleural pressure |
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What happens during pneumothorax?
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Air is introduced into the intrapleural space
This causes the intrapleural pressure to equal atmospheric pressure The lungs follow their natural tendency to collapse The chest wall follows its natural tendency to expand |
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What happens to lung compliance in a patient with emphysema?
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Lung compliance increases because the alveoli are eaten away
The tendency of the lungs to collapse is decreased A new, higher FRC is established because air can't escape The chest becomes barrel-shaped |
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What happens to lung compliance in a patient with fibrosis?
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Lung compliance decreases
The tendency of the lungs to collapse is increased A new, lower FRC is established because the tendency of the lungs to collapse exceeds the tendency of the chest wall to expand |
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What causes surface tension in the alveoli?
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Attractive forces between liquid molecules lining the alveoli
This creates a collapsing pressure that is directly proportional to surface tension and inversely proportional to alveolar radius |
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Laplace's Law
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P = 2T/r
P = collapsing pressure (pressure required to keep alveolus open) T = surface tension R - radius of alveolus |
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How does collapsing pressure vary according to alveolar radius?
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Large alveoli (large radius) have low collapsing pressures, so it is easy to keep them patent
Small alveoli (small radius) have high collapsing pressures, and are easier to collapse |
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What is atelectasis?
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Alveolar collapse
|
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What happens if there is no surfactant?
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Small alveoli have a tendency to collapse (atelectasis)
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How does surfactant reduce alveolar surface tension?
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Disrupts the intermolecular forces between liquid molecules
This prevents small alveoli from collapsing and increases compliance |
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How is surfactant produced?
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It is made by type II alveolar cells
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What is surfactant made of?
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Comprised mostly of the phospholipid dipalmitoyl phosphatidylcholine (DPPC)
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When during fetal development is surfactant produced?
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This is somewhat variable
Can be made as early as 24 weeks Almost always present by 35 weeks A lecithin:sphingomyelin ratio greater than 2:1 in the amniotic fluid generally reflects mature levels of surfactant |
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What is neonatal respiratory distress syndrome?
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Occurs in premature infants who have not manufactured sufficient amounts of surfactant
These infants have atelectasis (collapsed lungs), difficulty reinflating the lungs because of decreased compliance, and hypoxemia (decreased V/Q) |
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What drives airflow?
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The pressure difference between the mouth or nose and the alveoli
|
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How is airflow related to airway resistance?
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Inversely proportional
The higher the airway resistance, the lower the airflow |
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Equation for airflow
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Q = delta P / R
Q = airflow delta P = pressure gradient R = resistance |
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Formula for airway resistance
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R = (8nl) / (pi x r^4)
n = viscosity l = length of airway r = radius |
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What is the relationship between airway resistance and radius of the airway?
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Resistance is inversely proportional to the fourth power of the airway
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What is the major site of airway resistance?
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Medium-sized bronchi
|
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What factors cause the bronchial smooth muscle to contract?
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Parasympathetic stimulation
Irritants Slow-reacting substance of anaphylaxis (asthma) |
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What factors cause the bronchial smooth muscle to relax?
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Sympathetic stimulation
Sympathetic agonists These things use beta 2 receptors |
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How does isoproterenol affect bronchodilation?
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It is a sympathetic agonist, and this causes the bronchioles to dilate
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How does lung volume contribute to airway resistance?
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Lung tissue exerts radial traction upon the airways
High lung volumes are associated with greater traction and decreased resistance Low lung volumes exert less traction, and there can be resistance to the point of airway collapse |
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How do the density and viscosity of an inspired gas affect airflow?
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They change the resistance to airflow
During deep-sea diving, air density increases and resistance increases Low-density gases such as helium reduce airflow resistance |
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What are the thoracic pressures at rest, before inspiration begins?
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Alveolar pressure = atmospheric pressure = 0
Intrapleural pressure is negative due to the opposing forces of the lungs trying to collapse and the chest wall trying to expand |
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Equation for airflow
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Q = delta P / R
Q = airflow delta P = pressure gradient R = resistance |
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Formula for airway resistance
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R = (8nl) / (pi x r^4)
n = viscosity l = length of airway r = radius |
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What is the relationship between airway resistance and radius of the airway?
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Resistance is inversely proportional to the fourth power of the airway
|
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What is the major site of airway resistance?
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Medium-sized bronchi
|
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What factors cause the bronchial smooth muscle to contract?
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Parasympathetic stimulation
Irritants Slow-reacting substance of anaphylaxis (asthma) |
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What factors cause the bronchial smooth muscle to relax?
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Sympathetic stimulation
Sympathetic agonists These things use beta 2 receptors |
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How does isoproterenol affect bronchodilation?
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It is a sympathetic agonist, and this causes the bronchioles to dilate
|
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How does lung volume contribute to airway resistance?
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Lung tissue exerts radial traction upon the airways
High lung volumes are associated with greater traction and decreased resistance Low lung volumes exert less traction, and there can be resistance to the point of airway collapse |
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How do the density and viscosity of an inspired gas affect airflow?
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They change the resistance to airflow
During deep-sea diving, air density increases and resistance increases Low-density gases such as helium reduce airflow resistance |
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What are the thoracic pressures at rest, before inspiration begins?
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Alveolar pressure = atmospheric pressure = 0
Intrapleural pressure is negative due to the opposing forces of the lungs trying to collapse and the chest wall trying to expand |
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Which of the standard lung volumes is in the lungs at rest?
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The FRC
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What happens to the thoracic pressures during inspiration?
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The inspiratory muscles contract and increase the thoracic volume
This causes the intrapleural pressure to become more negative The increased transmural pressure on the alveoli causes the alveolar pressure to become negative The pressure gradient between the alveoli and the air causes air to flow into the lungs |
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How does lung volume relate to elastic recoil?
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Elastic recoil is greatest when the lungs contain high volumes
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What do we measure when we want to know about the dynamic compliance of the lungs?
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Changes in intrapleural pressure during inspiration
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Which of the standard lung volumes is in the lungs at the peak of inspiration?
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FRC + TV
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What happens to the thoracic pressures during expiration?
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The inspiratory muscles relax and the thoracic pressure becomes less negative
This causes the alveolar pressure to become positive The pressure gradient causes air to flow from the lungs out the airway |
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What happens to intrapleural pressure during a forced expiration?
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It becomes POSITIVE
During quiet expiration, IPP becomes less negative, but never actually becomes positive Positive IPP can compress the airways and make expiration more difficult |
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How is breathing altered in a patient with COPD?
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Airway resistance is increased
Patients learn to expire slowly with pursed lips This prevents the airway collapse that can occur with a forced expiration |
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Which of the standard lung volumes is in the lungs at the end of a quiet expiration?
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The FRC
|
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What is asthma?
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An obstructive disease where expiration is impaired
Patients have low FEV1/FVC Air that should be expired is instead getting trapped, which causes the FRC to increase |
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What is COPD?
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A combination of chronic bronchitis and emphysema
Obstructive disease with increased lung compliance, so expiration is impaired Decreased FEV1/FVC Air that should be expired is trapped, leading to increased FRC and a barrel-shaped chest |
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What are "pink puffers?"
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COPD patients who primarily have emphysema
Mild hypoxemia Normocapnia because alveolar ventilation is maintained |
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What are "blue boaters?"
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COPD patients who primarily have bronchitis
Severe hypoxemia with cyanosis Hypercapnia because alveolar ventilation is not maintained Right ventricular failure and systemic edema |
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What is fibrosis?
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Restrictive disease associated with decreased lung compliance, so inspiration is impaired
All lung volumes are decreased FEV1/FVC is increased |
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What is Dalton's law of partial pressure?
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Partial pressure = total pressure x fractional gas concentration
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What is the fractional concentration of oxygen in dry inspired air?
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21%
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When calculating the partial pressure of oxygen in humidified tracheal air, what do we have to do to calculate?
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You have to subtract the partial pressure of water (47 mmHg) from the total pressure before multiplying by the fractional concentration of oxygen
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Are the systemic and pulmonary circulations entirely separate?
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No
2% of cardiac output bypasses the pulmonary circulation (physiologic shunt), and this venous blood mixes with arterial blood This makes the PO2 of arterial blood slightly lower than the PO2 of alveolar air |
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How much gas dissolves in solution?
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An amount that is proportional to the partial pressure
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Formula for dissolved gas in solution
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Dissolved gas = partial pressure of gas x solubility in blood
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What factors impact the diffusion rates of O2 and CO2?
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The partial pressure difference across the membrane
The surface area available for diffusion |
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What gases exhibit perfusion-limited exchange?
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N2O
O2 (under normal conditions) |
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What is perfusion-limited exchange?
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The gas equilibrates early along the length of the pulmonary capillary
The partial pressures of the gas in the arterial blood and alveolar air become equal Diffusion of the gas can be increased only if blood flow increases |
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What gases exhibit diffusion-limited exchange?
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CO
O2 (emphysema, fibrosis, and during strenuous exercise) |
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What is diffusion-limited exchange?
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The gas does not equilibrate by the time the blood reaches the end of the pulmonary capillary
The partial pressure difference of the gas between the arterial blood and the alveolar air is maintained Diffusion continues as long as there is a partial pressure gradient |
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How does fibrosis cause O2 to become diffusion-limited?
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Thickening of the alveolar membrane increases diffusion distance
This restricts the diffusion of O2 |
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How does emphysema cause O2 to become diffusion-limited?
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The surface area for gas diffusion is decreased
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How is oxygen transported in the blood?
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Dissolved
Bound to hemoglobin (most important mechanism) |
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What is the structure of adult hemoglobin?
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Globular tetramer
Each subunit has a heme moiety, which is iron-containing porphyrin The iron is in the ferrous 2+ state, which binds oxygen If the iron is in the ferric 3+ state, it is methemoglobin and will not bind oxygen Made of 2 alpha and 2 beta chains (normal adult Hb is known as a2B2) |
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What is the structure of fetal hemoglobin?
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The beta chains are replaced by gamma chains, so fetal Hb is known as a2y2
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What is the difference in oxygen affinity between adult and fetal hemoglobin?
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Fetal Hb has higher oxygen affinity
This means the oxygen dissociation curve is left-shifted relative to the adult curve Because of this phenomenon, a fetus will draw maternal oxygen across the placenta |
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How do fetal and adult hemoglobins differ with regard to 2,3-BPG binding?
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Fetal Hb binds 2,3-BPG less avidly
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What is the oxygen-binding capacity of blood?
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The maximum amount of O2 that can be bound to hemoglobin in the blood
Is dependent upon the hemoglobin concentration of the blood Limits the amount of O2 that can be carried in the blood |
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What is the oxygen content of the blood?
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The total amount of oxygen carried in blood, including Hb-bound and dissolved
Depends upon the Hb concentration, PO2, and the P50 of Hb |
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Formula for oxygen content
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O2 content = (oxygen binding capacity x %saturation) + dissolved O2
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What is the name of hemoglobin that is bound to oxygen?
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Oxyhemoglobin
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What is the percent saturation of Hb at 100 mmHg (arterial blood)?
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100% saturated
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What is the percent saturation of Hb at 40 mmHg (mixed venous blood)?
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75% saturated
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What is the percent saturation of Hb at 25 mmHg?
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25% saturated
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What is the shape of the oxygen dissociation curve?
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Sigmoidal
This is because the affinity of hemoglobin increases as each successive oxygen molecule binds a heme (this is positive cooperativity) |
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How does the sigmoidal shape of the oxygen dissociation curve affect oxygen loading and unloading?
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Changing oxygen affinity facilitates oxygen loading in the lungs, and unloading in the tissues
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Why can people tolerate changes in atmospheric pressure and oxygen without compromising the oxygen-carrying capacity of Hb?
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Because the oxygen dissociation curve is almost flat between PO2 of 60 and 100 mmHg
However, below 60, the slope decreases sharply and small decreases in oxygen produce large changes in oxygen-carrying capacity |
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What happens to oxygen and hemoglobin in the lungs?
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Oxygen diffuses from alveolar gas to pulmonary capillary blood
The PO2 of alveolar gas is 100 mmHg, and oxygen affinity of Hb is very high at this concentration This facilitates the diffusion process By tightly binding oxygen, the free oxygen concentration and O2 partial pressure are kept low, which maintains the partial pressure gradient |
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What happens to oxygen and hemoglobin in the peripheral tissues?
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O2 diffuses from the arterial blood to the cells
The gradient for diffusion is maintained because the cells consume O2 for metabolism, which keeps the tissue PO2 low The lower affinity of Hb for O2 in this portion of the curve facilitates O2 unloading |
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What factors cause the oxygen dissociation curve to be shifted to the right (that is, decrease the affinity of hemoglobin for O2)?
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Increased PCO2
Decreased pH Increased temperature Increased 2,3-BPG concentration |
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What is an adaptation to chronic hypoxemia at high altitudes?
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Increased production of 2,3-BPG to facilitate oxygen unloading in the tissues
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What factors cause the oxygen dissociation curve to be shifted to the left (increase the affinity of hemoglobin for O2)?
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Decreased PCO2
Increased pH Decreased temperature Decreased 2,3-BPG concentration |
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Under what conditions is oxygen loading and unloading onto hemoglobin most difficult?
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Under conditions that left-shift the oxygen dissociation curve
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How does CO binding to hemoglobin affect O2 binding?
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CO competes with O2 for binding sites
Hb's affinity for CO is 200X higher than its affinity for O2 CO binds to Hb and decreases the O2 concentration of the blood CO binding to Hb increases the affinity of the remaining Hb sites for O2, so this shifts the oxygen dissociation curve to the left |
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What is hypoxemia?
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Decreased arterial PO2
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What is the A-a gradient?
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The difference between arterial and alveolar air PO2 concentrations
|
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Formula for A-a gradient
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Gradient = alveolar air PO2 - arterial PO2
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Formula for alveolar air PO2
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Alveolar air PO2 = PIO2 - [arterial PCO2 / R)
PIO2 = PO2 of the inspired air R = 0.8 usually |
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What is the normal A-a gradient
|
Less than 10 mmHg because O2 normally equilibrates between alveolar gas and arterial blood
If the gradient is increased, something is inhibiting equilibration (diffusion defect, V/Q defect, R-to-L shunt) |
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What is hypoxia?
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Decreased oxygen delivery to the tissues
|
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Formula for oxygen delivery
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O2 deliver = cardiac output x O2 content of blood
|
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How is CO2 transported in the blood?
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Dissolved
Bound to hemoglobin (carbaminohemoglobin) Bicarbonate (major form of transport) |
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How is CO2 transported as bicarbonate?
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CO2 is generated in the tissues, and it diffuses into the RBCs
Carbonic anhydrase generates H + HCO3 HCO3 leaves the RBCs in exchange for Cl; this is known as the chloride shift HCO3 is transported to the lungs in plasma In the lungs, HCO3 goes back into RBCs in exchange for Cl and carbonic anhydrase catalyzes the reverse reaction CO2 diffuses out of the RBCs and is expired |
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How is H buffered inside RBCs?
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It is buffered by deoxyhemoglobin (Hb with no O2)
DeoxyHb is a better buffer than oxyHb (oxygen-bound Hb), so it is helpful that blood has been deoxygenated by the time it reaches the venous end of the capillaries |
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How does pulmonary circulation pressure compare to systemic circulation pressure?
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It is much lower (about 15 mmHg in the pulmonary artery vs 100 mmHg in the aorta)
|
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How does pulmonary circulation resistance compare to systemic circulation resistance?
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Resistance is much lower in pulmonary circulation
|
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What is the distribution of blood in the lung in the supine and standing positions?
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Supine -- evenly distributed
Standing -- blood tends to move downward due to gravity |
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What are the zones of the lung?
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Zone 1 -- apex of the lung
Zone 2 -- middle of the lung Zone 3 -- base of the lung |
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Which zones of the lung have the lowest and highest blood flow when standing?
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Zone 1 has the lowest flow because of gravity
Zone 3 has the highest flow |
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What is the order of the alveolar, arterial, and venous pressures (from highest to lowest) in zone 1 of the lung?
|
Alveolar > arterial > venous
|
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What is the order of the alveolar, arterial, and venous pressures (from highest to lowest) in zone 2 of the lung?
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Arterial > alveolar > venous
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What is the order of the alveolar, arterial, and venous pressures (from highest to lowest) in zone 3 of the lung?
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Arterial > venous > alveolar
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How does high alveolar pressure affect blood flow in zone 1 of the lung?
|
It may compress the capillaries and reduce blood flow
This can occur if arterial pressure is decreased from hemorrhage Can also occur if positive-pressure ventilation has artificially increased the alveolar pressure |
|
What happens to arterial pressure as you move down the lung?
|
It increases due to hydrostatic pressure
|
|
What is hypoxic vasoconstriction?
|
Hypoxia causes vasoconstriction (unlike in other organs, where hypoxia causes vasodilation)
This directs blood away from poorly ventilated regions |
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How much pulmonary vascular resistance is observed in the developing fetus?
|
A lot
This is because of generalized hypoxic vasoconstriction Therefore, blood flow through the fetal lungs is low |
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What happens to fetal lungs when the first breath begins?
|
The alveoli become oxygenated
Pulmonary vascular resistance decreases Pulmonary blood flow increases and becomes equal to cardiac output |
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What type of cardiac shunt is seen in tetralogy of Fallot?
|
Right to left
|
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What is the effect of a right-to-left cardiac shunt upon arterial PO2?
|
Decreases PO2 because there is mixture of venous and arterial blood
|
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What type of cardiac shunt is most common and why?
|
Left to right, because pressures are higher on the left side of the heart
|
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What is the effect of a left-to-right cardiac shunt upon arterial PO2?
|
Arterial PO2 does not change
Venous blood PO2 increases because oxygenated blood is diverted to the right side of the heart |
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What is the V/Q ratio?
|
The ratio of alveolar ventilation to perfusion
Ideal exchange of O2 and CO2 depends upon ventilation and perfusion matching |
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What is the approximate V/Q ratio in a normal healthy patient
|
0.8
|
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In what zone of the lung is ventilation the highest?
|
zone 3
|
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In what zone of the lung is V/Q highest? Lowest?
|
Highest in zone 1
Lowest in zone 3 |
|
How does V/Q affect gas exchange in the different regions of the lungs?
|
The apex (zone 1) has the highest V/Q, so there is more gas exchange. Therefore, PO2 is highest and PCO2 is lowest here
In the base (zone 3), V/Q is lower so there is less gas exchange, resulting in the lowest PO2 and highest PCO2 |
|
How does airway obstruction alter the V/Q ratio?
|
V = 0, so V/Q = 0
This is a shunt |
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What is the status of gas exchange in a region of the lung that is perfused but not ventilated?
|
There is no gas exchange
V/Q = 0 Therefore, PO2 and PCO2 of the capillary blood approach their values in venous blood |
|
What happens to the A-a gradient if there is an airway obstruction?
|
It increases because gas exchange is decreased
|
|
What happens to V/Q when there is a circulatory obstruction?
|
This can happen in a pulmonary embolism
Q = 0, so V/Q is infinite When V/Q is infinite, you have dead space |
|
What are the PO2 and PCO2 values of alveolar gas when the lung is ventilated but not perfused?
|
They approach their values in inspired air
|
|
What part of the CNS contains the various centers that neurally control respiration?
|
Sensory information (PCO2, lung stretch, irritants, etc) is coordinated in the brain stem
Brain stem output controls respiratory muscles and the breathing cycle |
|
What are the respiratory centers?
|
Medullary respiratory center -- reticular formation
Apneustic center -- lower pons Pneumotaxic center -- upper pons Cerebral cortex |
|
What respiratory groups are found in the respiratory medullary centers?
|
Dorsal respiratory group
Ventral respiratory group |
|
What does the dorsal respiratory group of the medullary respiratory center do?
|
Responsible for inspiration
Generates the basic rhythm for breathing Input to the DRG comes from the vagus (peripheral chemoreceptors, lung mechanoreceptors) and glossopharyngeal (peripheral chemoreceptors) nerves Output from the DRG travels via the phrenic nerve to the diaphragm |
|
What does the ventral respiratory group of the medullary respiratory center do?
|
Primarily responsible for active expiration
Not active during quiet breathing |
|
What does the apneustic center do?
|
Stimulates deep and prolonged inspiratory gasps (apneusis)
|
|
What does the pneumotaxic center do?
|
Inhibits inspiration to regulate respiratory volume and respiration rate
|
|
What does the cerebral cortex do (in the context of breathing)?
|
Allows you to voluntarily control your breathing to a certain extent
Voluntary hypoventilation is limiting by increasing PCO2 |
|
What are the types of chemoreceptors?
|
Central chemoreceptors in the medulla
Peripheral chemoreceptors in the carotid and aortic bodies |
|
How do the central chemoreceptors work?
|
Sensitive to the pH of the CSF
Decreased pH stimulates hyperventilation Increased pH stimulates hypoventilation |
|
How is low pH detected in the CSF?
|
H does not cross the blood-brain barrier very well, but CO2 does
In the CSF, CO2 reacts with water to give H and HCO3 It is this H that is detected by the central chemoreceptors |
|
How do the peripheral chemoreceptors work?
|
Decreased arterial PO2 causes hyperventilation
Increased arterial PCO2 causes hyperventilation Arterial H stimulates the carotid body receptors directly to cause hyperventilation |
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In addition to chemoreceptors, what other types of sensory receptors are involved in the control of breathing?
|
Lung stretch receptors
Irritant receptors J (juxtacapillary receptors) Joint and muscle receptors |
|
How do lung stretch receptors work?
|
Found in the smooth muscle of the airways
When these receptors are stimulated by stretch, they decrease breathing frequency |
|
What is the Hering-Breuer reflex?
|
Increased lung volume (stimulation of stretch receptors) causes a decrease in breathing frequency
|
|
How do irritant receptors work?
|
Found between airway epithelial cells
Stimulated by noxious substances |
|
How do J receptors work?
|
Found in the alveolar walls
Engorgement of pulmonary capillaries stimulates them and causes rapid, shallow breathing |
|
How do the joint and muscle receptors work?
|
They are activated during limb movement
Involved in the early stimulation of breathing during exercise |
|
What happens to gas exchange during exercise?
|
Increased ventilatory rate, probably via joint and muscle receptors
This increases gas exchange in a given time period Increased oxygen consumption Increased CO2 production |
|
What happens to arterial and venous blood gas values during exercise?
|
Mean arterial PO2 and PCO2 do not change
Arterial pH doesn't usually change, but severe exercise can cause lactic acidosis Venous PCO2 increases because this is where exercise-produced CO2 is carried |
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What happens to V/Q during exercise?
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Cardiac output increases and this increases pulmonary blood flow
More pulmonary capillaries are perfused and more gas exchange occurs The distribution of V/Q throughout the lung becomes more even and there is a decrease in physiologic dead space |
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What are some adaptations to high altitude?
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Decreased alveolar PO2, resulting in hypoxemia
Hypoxemia stimulates hyperventilation Hypoxemia also stimulates RBC production, which increases the Hb concentratio in the blood More 2,3-BPG is produced to right-shift the oxygen dissociation curve Pulmonary vasoconstriction due to hypoxemia, causing increased pulmonary arterial pressure and hypertrophy of the right ventricle |
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What is acetazolamide used for?
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Treatment of respiratory alkalosis from hyperventilation at high altitudes
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