PHS 3342 Lecture Notes - Lecture 14: Alveolar Pressure, Thrombus, California State Route 2
28 Apr 2018
School
Department
Course
Professor
March 23, 2018
Respiratory Physiology
Ventilation
Ventilation: rate of air exchange
-Allows us to consider the link that exists between the bulk flow of air and the molecular events of gas exchange
Anatomical Dead Space
With each breath, part of the air we inhale does not reach the alveoli
-As such, it is not useful in gas exchange and is therefore called “dead space”
Anatomical dead space: volume of air that does not participate in gas exchange because it remains in the conducting
airways (not surrounded by capillaries)
-1 mL/pound of body weight
Estimated by measuring [N2]
-Patient exhales completely then inhales deeply from 100% oxygen gas mixture
-Patient breathes out
-Anatomic dead space = volume exhaled during first phase (containing 0% N2) + ½ exhaled during second phase
(transition from pure dead space air to pure alveolar air)
Physiological Dead Space
PDS = anatomical dead space + alveolar dead space
-Alveolar dead space represents alveoli not participating in gas exchange
•Not an ideal situation
•Ex. Blood clot blocking blood flow to alveoli
VD/VT = (PACO2 - PECO2)/PACO2
-VD = anatomical dead space
-VT = tidal volume
-PECO2 = partial pressure of CO2 exhaled
-VD/VT can be used to represent physiological dead space
Alveolar Ventilation (VA)
Dead space volumes must be subtracted from tidal volume to identify the true volume of air that participates in
meaningful gas exchange (alveolar ventilation)
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March 23, 2018
Factors Determining Alveolar Gases
pACO2: alveolar CO2 levels are:
-Directly influenced by the rate of CO2 production in the body VCO2
•~200 mL/min
-Inversely proportional to alveolar ventilation (VA)
-pACO2 often approximated as ~paCO2
-pACO2 ∝ VCO2/VA
pAO2
-Estimated using the alveolar gas equation
•
•A = alveolar, i = inspired, a = arterial
•R = metabolic quotient = CO2 produced/O2 consumed = 0.8 (can vary according to the energy source used by
tissues)
-*Don’t need to know how to calculate it, just use 0.8
-Usually ~100 mmHg
Hyperventilation
Leads to decreased pACO2 and increased pAO2
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March 23, 2018
But, increasing pO2 much above normal levels (100 mmHg) doesn’t do too much - oxygen dissolved in blood doesn’t
have a big effect, most oxygen is carried on hemoglobin
Biggest benefit is getting rid of more CO2 - not much oxygen will actually be increased
Hypoventilation
Leads to increased pACO2 and decreased pAO2
Usually due to a disease state, you can’t really decrease your breathing rate that much normally
NB: only ventilation can decrease pACO2; low pAO2 can be increased by increased piO2
Ventilation and Perfusion
The efficiency of the lung as an “aerator” of the blood easing through the pulmonary circulation clearly depends upon
appropriate matching of:
-Ventilation (i.e. air flow into a group of alveoli)
-Perfusion (i.e. blood flow in the capillaries surrounding those alveoli)
One example of an extreme deviation from a perfect matching of these parameters is physiological dead space
where alveoli are ventilated but not perfused
Both ventilation and perfusion are under a degree of local control due to the sensitivity of the smooth muscle of the
bronchioles and of the blood vessels of the pulmonary circulation to the pO2 (and pCO2) of the air and of the blood
The inequality of ventilation:perfusion ratio may be exaggerated either in the case of a partial airway obstruction or by
changes in blood flow such as may be encountered in different regions of “zones” of the lung due to different levels of
hydrostatic pressure
Ventilation (V)
At apex: less ventilation and perfusion
-Intrapleural pressure is more negative
-Greater transmural pressure
-Large alveoli
-Lower intravascular pressure
-Less blood flow
Alveoli at the top of the lung are more expanded (because of the lower intrapleural pressure) and therefore undergo a
smaller change in volume (ventilation) during inspiration
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Document Summary
Allows us to consider the link that exists between the bulk ow of air and the molecular events of gas exchange. With each breath, part of the air we inhale does not reach the alveoli. As such, it is not useful in gas exchange and is therefore called dead space . Anatomical dead space: volume of air that does not participate in gas exchange because it remains in the conducting airways (not surrounded by capillaries) Patient exhales completely then inhales deeply from 100% oxygen gas mixture. Anatomic dead space = volume exhaled during rst phase (containing 0% n2) + exhaled during second phase (transition from pure dead space air to pure alveolar air) Pds = anatomical dead space + alveolar dead space. Alveolar dead space represents alveoli not participating in gas exchange: not an ideal situation, ex. Peco2 = partial pressure of co2 exhaled. Vd/vt can be used to represent physiological dead space.
