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The role of equal pressure points in understanding pulmonary diseases

Article  in  AJP Advances in Physiology Education · September 2013

DOI: 10.1152/advan.00014.2013 · Source: PubMed

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Illuminations
The role of equal pressure points in understanding pulmonary diseases
P. J. G. M. Voets1 and H. A. C. van Helvoort2
1
Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands; and 2Department of Pulmonary Diseases,
Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
Submitted 4 February 2013; accepted in final form 14 May 2013
THE RESPIRATORY SYSTEM is composed of a conducting part and a
respiratory part. The conducting airways, i.e., the trachea, bronchi,
and bronchioles, differ in architecture. Both trachea and bronchi
are surrounded by rings of hyaline cartilage for support, whereas
the bronchiolar wall does not contain any cartilage and therefore
tends to collapse in response to changes in intrapleural or airway
pressure. As a result of airflow resistance, pressure that is gener-
ated in the alveoli drops along the airways during expiration (1, 3).
This is also known as friction loss. When airway pressure has
dropped to a level where it equals intrapleural pressure during
forced expiration, an equal pressure point (EPP) is reached (4). At
the EPP, airways that are not supported by cartilage will collapse
(Fig. 1). In healthy lungs, the EPP will be reached in cartilaginous
airways as a result of sufficient alveolar driving pressure and only
a gradual drop in pressure due to minimal airway resistance (4). In
the case of (severe) airway obstruction, resistance to airflow will
be much greater, and the pressure drop will be much steeper. The
EPP will move upstream toward the alveoli and will be reached in
the thin-walled bronchioles, causing airway collapse and the typ-
ical depression in the flow-volume curve (2, 3).
Although the clinical importance of EPPs, especially in
obstructive airway diseases, is unquestionable, relatively little
effort has been put into a comprehensible description of the
dynamics involved in this phenomenon. This is unfortunate,
because correctly applying complex physics in a clinical con-
text can be a difficult task. Therefore, this report aimed to
provide a straightforward mathematical approach to the con-
cept of EPPs in the airways by combining important principles
of airflow dynamics in a conceivable way. This results in an
equation (Eq. 1) that can be used to get a better understanding
of how airflow and airway properties alter the tendency of
airways to collapse:
Tr2
L⫽ (1)
4␩Rv
where L is length, T is wall tension, r is the cross-sectional
radius of a segment, ␩ is viscosity, R is the alveolar radius, and
v is velocity.
The derivation of Eq. 1 will be discussed stepwise in this
article. Table 1 shows a glossary of the parameters.
Mathematical approach. Alveolar pressure (Palv) is the re-
sult of recoil pressure (Prec), created by expansion of the
alveoli, and intrapleural pressure (Ppl) and produces the driving
force for airflow through the respiratory system (2– 4). Accord-
ing to Pascal’s law, pressure will be dispersed equally in all
directions throughout the enclosed intrapleural cavity. There-
Address for reprint requests and other correspondence: H. A. C. van
Helvoort, Dept. of Pulmonary Diseases (454), Radboud Univ. Nijmegen
Medical Centre, PO Box 9101, Nijmegen 6500 HB, The Netherlands (e-mail:
H.vanHelvoort@long.umcn.nl).
266 1043-4046/13 Copyright © 2013 The American Physiological Society
Adv Physiol Educ 37: 266–267, 2013;
doi:10.1152/advan.00014.2013.
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Fig. 1. Schematic representation of the respiratory system, enclosed by the
intrapleural cavity. Alveolar pressure (Palv) is generated as a result of elastic
recoil due to wall tension (T) and intrapleural pressure (Ppl). Where the
pressure drop (⌬P) over a certain distance (L) from the alveoli equals recoil
pressure, an equal pressure point will arise. Cartilaginous airways (on the right
side) are barred.
fore, Ppl exerted on the alveoli will equal Ppl exerted on the
airways. Assuming that the alveoli are perfect spheres,
Laplace’s law (Eq. 2) can be used to describe Prec in terms of
R and T, which is the result of lung tissue elasticity and surface
tension (6):
2T
Prec ⫽ (2)
R
The equation for Palv (Eq. 3) can now be written as follows:
2T
Palv ⫽ Ppl ⫹ Prec ⫽ Ppl ⫹ (3)
R
As air flows during expiration, pressure inside the airways will
drop as a result of friction loss. The relationship between the
pressure drop (⌬P), resistance to airflow (RAW), and airflow
(⌽) is given by Poiseuille’s law (Eq. 4), which can be applied
to the laminar flow of Newtonian fluids (4, 6). Airflow be-
comes more turbulent as flow velocity and airway diameter
increase. Therefore, larger airways are much more prone to
turbulent flow than bronchiloles (5). To apply Poiseuille’s law,
laminar flow is assumed in the smallest airways in this model,
although even in bronchioles airflow will not be entirely
laminar during forced expiration. RAW depends on ␩, the
length of the airway segment through which air flows (L), and
the cross-sectional radius of this segment (r):
8␩L
⌬P ⫽ RAW⌽ ⫽ ⌽ (4)
␲r4
The continuity equation for ⌽ (Eq. 5) essentially states that
what goes in at one end of the airway segment must come out
at the other end. The volume of air (⌬V) that passes a certain
point per unit of time (⌬t), i.e., the flow, will not change.
 Illuminations
267

Table 1. Glossary of parameters nary EPP. The equation that has been derived in this article
(Eq. 1) shows that as the value of L decreases, the EPP moves
Parameter Definition away from the cartilaginous airways toward the alveoli, caus-
␩ Viscosity ing an obstruction to airflow as soon as the EPP moves to a
⌽ Airflow collapsible region of the airway. This can be illustrated by the
A Cross-sectional area of the airways altered airflow dynamics in a number of pulmonary diseases (3,
EPP Equal pressure point 4). In asthma and chronic obstructive pulmonary disease, for
L Length
Palv Alveolar pressure instance, airway inflammation reduces r (increasing RAW) and
Prec Recoil pressure therefore reduces the distance from the alveolus to the EPP.
r Cross-sectional radius of the segment The same effect on L can be seen in emphysema, as a result of
R Alveolar radius the decrease in T and an increase in r, due to the disintegration
RAW Resistance to airflow
T Wall tension of alveolar septa. Conversely, pursed lip breathing (which is
v Velocity commonly used instinctively by persons suffering from chronic
obstructive pulmonary disease) decreases v, increasing the
airway pressure, which moves the EPP downstream toward the
Therefore, an increase in cross-sectional area of the airways

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cartilaginous airways, preventing collapse.
(A) is accompanied by a decrease in v (6): Taken together, it is important to note that it is not the aim of
⌬V ⌬x this equation to calculate EPP positions exactly, and it should not
⌽⫽ ⫽A ⫽ Av ⫽ ␲r2v ⫽ constant (5) be used for this purpose. Rather, the derived equation should be
⌬t ⌬t considered a means for students or clinicians to get a better
This result (Eq. 6) can be combined with Poiseuille’s law (Eq. 4) understanding of how (changes in) relevant parameters influence
as follows: the tendency of airways to collapse in pulmonary disease.
8␩L 8␩Lv
⌬P ⫽ RAW⌽ ⫽ ␲r2v ⫽ (6) DISCLOSURES
␲r 4
r2 No conflicts of interest, financial or otherwise, are declared by the author(s).
As mentioned above, an EPP will arise where airway pressure
has dropped to a level where it equals Ppl (4). Airway pressure AUTHOR CONTRIBUTIONS
at distance L from the alveoli is defined as Palv minus ⌬P over Author contributions: P.V. conception and design of research; P.V. ana-
L, as follows: lyzed data; P.V. and H.v.H. interpreted results of experiments; P.V. prepared
figures; P.V. and H.v.H. drafted manuscript; P.V. and H.v.H. approved final
2T version of manuscript; H.v.H. edited and revised manuscript.
Palv ⫺ ⌬P ⫽ Ppl ⫹ ⫺ ⌬P ⫽ Ppl (7)
R
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