Pulmonary Physiology II Flashcards
The thickness of the normal alveolar-capillary barrier is
Small (0.3 um)
The surface area in the lungs and tissues is huge and is proportional to
Capillary density
Therefore, under normal circumstances, O2 and CO2 diffuse very rapidly, allowing for very efficient
Gas-exchange
The diffusing capacity of the lungs is clinically measured by determining the
Diffusion capacity of carbon monoxide (DLCO)
Used to determine diffusing capacity of the lungs because its partial pressure in capillary blood is essentially zero under normal conditions and it diffuses very rapidly
CO
Basically the test involves having the patient breathe in a very small known percentage of CO in air, hold their breath for a few seconds; then the expired air is collected, and remaining CO in the expelled sample is
Measured
Exercise in a healthy person would increase
DLCO
Thickening of the diffusion barrier, decreased surface area, reduced uptake by erythrocytes, and ventilation perfusion mismatch cause
Decrease in DLCO
Thickening of the diffusion barrier can be caused by
Edema and fibrosis
Decreased surface area can be caused by
Emphysema and decreased cardiac output
Reduced uptake by erythrocytes can be caused by
Anemia
The pressure of a gas if it occupied the total volume in absence of other gas components
Partial pressure of a gas
Partial pressure is proportional to
Concentration of the gas
What is the PO2 of inspired air at see level?
150 mmHg
The partial pressure of a gas in liquid (Pgas) is its partial pressure in a gas mixture in equilibrium with the
Solution
Normally alveolar PO2 and PCO2 equilibrate with
Pulmonary capillary blood
Partial pressure measurement is important because gs passes through membranes in
Dissolved form
Represent dissolved gasses, that is, gasses that are not bound to Hb
Blood partial pressure
What is the Pi(inspired)O2
150 mmHg
What is alveolar O2 Pressure (PAO2)
100 mmHg
What is PACO2?
40 mmHg
What is the arterial O2 pressure (PaO2)?
95-98 mmHg
What is PaCO2?
40 mmHg
What is the venous partial pressure of CO2 (PvCO2)?
45 mmHg
What is PvO2?
40-45 mmHg
There is little arterial to venous difference in
CO2
Although lots of CO2 is produced and transported, the majority of the CO2 is in the form of
HCO3-
Shows the liters of air moved per unit time
-the way lung volumes are measured
Sirometry
The volume entering or leaving the nose or mouth per breath
-basal resting movement of volume
Tidal volume (VT)
The lung volume that results from a maximal inspiration following a normal inspiration
Inspiratory Capacity (IC)
The additional volume that can be forcefully expired after a normal expiration
Expiratory Reserve Volume (ERV)
The maximal volume that can be forcefully inspired following a tidal inspiration
Inspiratory Reserve Volume (IRV)
The volume of gas remaining in the lungs after a normal tidal expiration
Functional Residual Capacity (FRC)
Important volume because it allows for continuous gas exchange between breaths
Functional residual capacity (FRC)
This is an invaluable measurement since it enables lung volumes to be subdivided based upon spirometric measurements
FRC
Note that since FRC is the sum of residual volume and ERV, FRC can only be measured using
-Or a body plethsymography
Gas dilution techniques
The volume of gas that can be moved into and out of the lungs with maximal effort
Vital capacity (VC)
In other words, Vital Capacity (VC) is the maximal ispiratory volume plus the
Maximal expiratory volume
The volume remaining in the lungs after a maximal expiration
Residual Volume (RV)
The volume in the lungs after a maximal inspiration
Total lung capacity
The actual process of airflow can be determined by having a patient undergo a forceful expiration following a
Forceful inspiration
This procedure can be recorded to show the
Flow volume loop (air flow in L/s vs Volume in L)
The flow volume loop is clinically valuable in order to evaluate whether or not airflow is appropriate for a given
Lung Volume
The general pattern of normal flow-volume (be it inspiration or expiration) is a
Rapid increase in flow followed by a slowed phase of flow
In order to establish flow-volume, the patient undergoes a maximal expiration to establish
RV
From RV, maximal inspiratory effort creates a downward convex plot which is read from
Right ot left
Upon maximal inspiration (TLC), the patient generates a maximal expiratory effort which creates a transient and very rapi rise in flow with little accompanying change in
Volume
This rapid rise in flow with little change in volume is the
Peak Expiratory Flow (PEF)
The PEF represents which phase of expiration?
Effort-dependent phase
What this means is that more effort can induce a greater rate of flow early on during
-due to greater alveolar distension, lower alveolar pressure relative to atmospheric, and high intrapleural pressure
Expiration
Peak expiratory flow is followed by a gradual reduction (downslope) in flow and a concomitant decrease in
Lung Volume
This downslope in the plot is the
Forced Vital Capacity (FVC)
The downslope of this plot is the FVC, which represents the
Effort independent phase of forced expiration
In other words, due to decreasing alveolar diameter and a reduction in alveolar pressure, intrapleural pressure causes compression of the
Relatively compliant small airways
This compression of the relatively compliant small airways is known as
Dynamic Airway Compression
A greater expiratory effort can not further increase airflow during the
Effort-independent phase
FVC end with
RV
FVC ends with RV, and with this, one complete flow-volume loop has been
Established
Importantly, the volume that is expired during the FIRST SECOND of FVC is the
Forced Expiratory Volume (FEV1)
Deviations in FEV1, FVC, and FEV1/FVC are used to diagnose
Obstructive and restrictive lung diseases
The result of some pathologic process that impedes airflow
Obstructive disease
When inflammation and mucus production in asthma and chronic bronchitis clog the airways, we have an
Obstructive disease
Another obstructive lung disease is the reduction in lung elastic recoil that is characteristic of
Emphysema
Obstruction is identified by an abnormal REDUCTION in both
FEV1 and FEV1/FVC
Obstruction is somewhat alleviated by the use of
Bronchodilators such as B2 agonists albuterol or salmeterol
Results from a decrease in lung parenchymal and/or chest wall compliance which then restricts filling capacity of the lungs
Restrictive lung disease
Fibrosis, obesity, and inflammatory pathologies of the parenchyma are some causes of
Restrictive lung disease
Restrictive lung diseases are characterized by
Decreased lung compliance
FEV1 is generally normal or may be increased due to enhanced elastic recoil with
Restrictive disease Would not significantly alter the results of pulmonary function tests in restrictive disease
A reduction in PaO2
Hypoxemia
A reduction in tissue PO2 which drives SaO2 below 90%
Hypoxia
In general, Hypoxia is accompanied by a PaO2 of
Less than 60%
Detects O2 saturation (SaO2) which infers capillary blood Hb in an oxyhemoglobin conformation
Pulse Oximetry (Pulse OX)
Arterial Blood Gases (ABG) is generally taken from the radial artery and measures
PaO2, PaCO2, and arterial pH
Determines the cause of hypoxemia based on the difference between PAO2 and PaO2
Alveolar to arterial O2 difference (A-a)DO2
The aleveolar to arterial O2 difference (sometimes referred to as the A-a gradient), as the name implies, is simply the difference between
PAO2 and PaO2
What is the
- ) Fraction of inspired O2 (FiO2)
- ) Atmospheric pressure
- ) Atmospheric O2
- ) 0.21
- ) 760 mmHg (Patm)
- ) PO2 = 47 mmHg
The (A-a)DO2 is usually less than
-increases by about 20 mmHg between ages 20 and 70
20
The age corrected formula is
(Age/4) + 4
How do we use the age correction?
Compare calculated (A-a)DO2 to age corrected value
An elevated (A-a)DO2 means that the O2 that is reaching his alveoli is not effectively reaching his
Arterial Blood
Some pathologies that can result in hypoxemia with an increased (A-a)DO2 are
A right-to-left shunt or markedly increased cardiac output
Alveolar capillary transit time is too short to allow unloading of alveolar O2 to blood with
Markedly increased cardiac output
What do we know about the condition of hypoxemia with normal (A-a)DO2?
Both PAO2 and PaO2 are decreased
What two things can result in hypoxemia with a NORMAL (A-a)DO2?
Hypoventilation and high altitude
A characteristic pattern accompanying hypoventilation would be
Decreased PAO2 and PaO2 with increased PaCO2
Blood gas levels will be markedly different from alveolar levels if there is an abnormality in the tissue barrier that limits
Diffusion
PaO2 is normally around
95-98 mmHg
Normally the diffusion of O2 and CO2 re not limited by the diffusion barrier, but rather by
Perfusion
The rate at which blood transits alveolar capillaries
Perfusion
Normal capillary transit time for a RBC and its accompanying plasma is about
0.75-1.2 seconds
At rest, after about a quarter of a second, all of the O2 that can diffuse form the alveoli has done so and no further increase in
Blood PO2 can occur
The only physiologic way to increase blood O2 content (CaO2) is by increasing
Cardiac Output
Decreased by pushing more RBCs through alveolr capillary units for oxygenation per unit time
Perfusion
During vigorous physical demand, capillary transit time can be reduced to around
0.25 seconds
When capillary transmit time is reduced to 0.25 seconds, we allow for more RBCs per unit time to be
Oxygenated
Always pathologic and occurs as a result of abnormal thickening of the alveolar membrane, pulmonary edema, low atmospheric PO2, etc
Diffusion limitation
If gas in pulmonary capillry blood equilibrates with alveolar gas within 0.75 seconds, than we know gas transport is limited by
Perfusion
Normal PAO2 is
100mmHg
Capillary blood flow is slow enough that O2 in alveoli and pulmonary capillaries will equilibrate. This occurs because of a very substantial
PAO2 - PvO2 gradient (100 mmHg - 40 mmHg)
