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What happens to VA/Q as you go through the height of the lung?

In the normal upright lung, both ventilation and perfusion
favor dependent lung regions (Chaps. 6 and 7). These relationships
will be explored here to develop a fuller understanding
of their normal ranges and perturbations having clinical
importance (Fig. 8.1). Since both
.VA and .Q
change with lung
height, their alveolar ventilation perfusion ratio
increases exponentially from lung base to apex. In this situation,.VA/.Q<1
at the level of the diaphragm due to the heavy blood fl ow
through Zone 3 capillaries. With increasing height above the
heart of the upright lung, the
.VA/.Qratio rapidly passes through
1.0 toward higher values that could theoretically approach
infi nity (ie, the denominator = 0) if apical alveolar capillaries are actually in Zone 1 conditions.


What are some general principles concerning the oxygen levels of pulmonary artery blood and inhaled air?

Regardless of their cause, inequalities in
have a
direct bearing on the effi ciency of ventilation and the adequacy
of perfusion. In simplifi ed form, the extreme range of possible
situations is shown in Fig. 8.2. The structures shown represent
individual alveoli and their capillaries, or entire lung lobes,
with several basic principles the same. First, inspired gas is
well mixed and normally provides a suitable Po2 even when
diluted with alveolar air. Second, pulmonary arterial blood
is also homogenous as it enters the lungs with respect to its
mixed venous O2 content, C–Vo2. Under these conditions, the
open airway and patent blood vessel serving the central gas
exchange structure in this diagram offer no serious impediments
to ventilation or perfusion, and thus its
.VA/Q = 1.


What happens when ventilation is low but blood perfusion remains normal? What might cause this? What is the term for this? What is the result? Same questions but for the opposite situation.

The lung unit to the left in Fig. 8.2 has normal, unimpeded
blood perfusion, but its ventilation is low, due perhaps
to mucus, edema, or other cause for a narrowed airway. The end result of this unit with low.VA/.Q(1/10) is wasted cardiac output and a decrease in pulmonary venous blood O2 content, CPVo2. Such wasted blood fl ow is termed physiological shunt, with the end result no different than if this blood had passed through an anatomical shunt between the right ventricle
and left atrium. The lung segment to the right in Fig. 8.2 shows adequate (even excessive) ventilation compared to its reduced perfusion. The consequence of a high
(10/1) is
enriched O2 content in pulmonary veins (or at least no reduction),
although signifi cant ventilation is wasted and contributes
to physiological dead space. Such vascular occlusion
might occur by an embolism, clot, or other obstructive effect
within the blood vessel.


What does the calculated physiologic dead space include? What about the calculated physiologic shunt?

Later sections of this chapter and Chap. 9 present equations
to calculate a patient’s physiological dead space and
physiological shunt. It is important to emphasize that such
physiological estimates are made on living subjects and
include any anatomical defects that are only quantifi able by
autopsy. Thus, a calculated physiological dead space includes
the anatomical dead space of conducting zone airways (Chap. 4)
plus the volume of all alveoli whose ventilation vastly exceeds
their blood fl ow, that is
>100 (Table 8.1). Likewise,
a calculated physiological shunt as detailed in Chap. 9 includes
actual extra-pulmonary anatomical defects like PDA or PFO
(Chap. 7) that allow systemic blood to bypass the pulmonary
circulation plus any pulmonary arterial blood fl owing
through alveoli with inadequate ventilation, that is,
(Table 8.1). By these defi nitions, healthy subjects are those
whose physiological dead space and shunt do not exceed their
anatomical dead space and shunt.


Explain the Acute Hypoxic Pressor Response. What are the results when a small percentage of the lung is hypoxic? What about when a large percentage is hypoxic? When might each happen?

Beyond such large-scale adjustments between ventilationand perfusion, pulmonary arterioles constrict directly in response to reduced PAo2. This acute hypoxic pressor response (AHPR) is a refl ex unique to the pulmonary circulation, evident even in isolated lungs (Fig. 8.3). AHPR adaptively diverts blood from hypoxic alveoli to improve local
matching and minimize arterial hypoxemia for the entire lung.

The degree of fl ow diversion attributable to the AHPR
diminishes when the entire lung is experiencing hypoxia.
Hypoxic foci that are small or limited to particular lobes, as during
pneumonia, receive little perfusion because the AHPR shunts
their blood supply to less hypoxic alveoli. In such cases, PVR
may be normal for the lungs as a whole, PPA need not increase to
Q, and so the risk of edema is low (Chap. 7). However,
when alveolar hypoxia involves the entire lung, as at altitude, the
AHPR affects all alveolar units and PVR increases substantially.
In that situation, right heart output and lung blood fl ow can only
be maintained by large increases in PPA. If persistent, the resulting
pulmonary hypertension can lead to vascular remodeling,
enlargement of the right ventricle, and cor pulmonale, topics
that will be discussed in Chaps. 13 and 26.


What are normal results of the multiple inert gas technique? What does it measure?

It measures how much VA and Q are occurring at various alveoli with varying VA/Q ratios.These clearance data are compiled to estimate theproportion of ventilation and perfusion going to alveolar unitshaving various .
VA/.Q ratios, plotted on a log scale from 0.01 to
100 (Fig. 8.4).The area under either curve must equal the entire.VA or Q per minute. Thus, the apex of the ventilation curve indicates that ~1.5 L/min of
A went to alveoli with
ratios of
slightly more than 1.0; blood fl ow going to this same population
of alveoli also was about 1.5 L/min. As is apparent from
the super imposable curves,
Q were well matched
in this lung, and result in a highly effi cient pattern of arterial


Explain what the results of the multiple inert gas technique would be like in a pulmonary embolism and why?

Pulmonary embolism (PE) provides a useful example of
how the multiple inert gas technique detects .
Q abnormalities
(Fig. 8.5). Whereas normal lungs show well-matched .
Q curves centered over 1.0, within minutes of PE a substantial
fraction of .
is ventilating alveoli whose microvasculature
is occluded by blood clots, fat, or even the N2 in air. For
those units in this example, .
Q is ~8 while the remaining
is ventilating relatively over-perfused alveoli. Overall, the PE has
increased .
VA and
Q (see total area under those curves); hypoxemia
and acidosis caused by these mismatches have stimulated
breathing and increased dead space ventilation (
D, L/min).


explain how inert gas results can differentiate type A and type B emphysema.

Inert gas results for type A emphysema show that most
.Q goes to alveoli with .VA/.Q slightly less than 1.0, while
.VA serves both alveoli with adequate .VA/.Q (~1.0) and those with little fl ow (.VA/.Q >5.0) (Fig. 8.6). Such patients may maintain a normal Pao2, but their .VE is high due to increased physiological dead space. Type B patients have little wasted .VA since most gas ventilates intact alveoli, but they often deoxygenate because a large part of .Q is wasted perfusing alveoli where .VA/.Q <0.1 due to increased physiological shunt. Structurally these results make sense. Patients with type B disease lack
intermediate airways that guide ventilation toward intact
peripheral alveoli. Their airway resistance is high and cyanosis occurs due to physiological shunt. Persons with type A disease lack delicate structures that comprise terminal acini. Their airways provide adequate ventilation to distal lung regions that may be devoid of alveolar capillaries and so their volume adds to physiological dead space.


Explain the relationships between VD, VE, VA, and VT.

Given the preceding discussion, the importance of distinguishing
A from .
VD is clear and has led to several complementary
approaches to estimating them from available patient data. In
Chap. 4, .
VA was introduced by stating that each tidal breath VT
is the sum of its dead space volume VD plus its alveolar parenchymal
volume VA:
VT = VD + VA (each in mL or L)
VT · f = (VD + VA) · f (where f = breaths/min)
.VE = .VD + .VA (each in L/min)


Explain how V(A) is calculated using the alveolar ventilation equation.

E, the
D is diffi cult to measure directly in living
subjects and so .
VA cannot be determined by this equation
alone. An indirect measure of .
VA can be derived with two
assumptions. First, since VD equals that portion of VT that cannot participate in diffusive gas exchange, all expired CO2 must originate in VA. Second, alveolar FAco2 = FEco2, measured as expiration approaches RV and exhaled gas is no longer diluted by dead space with its low [CO2] (Fig. 8.7). From these assumptions, a measured .Vco2 must equal the product ofan unknown
.VA (L/min) multiplied by estimated FAco2:

.Vco2 (L of CO2/min) =.VA (L of air/min) · FAco2 (L of CO2/Lof air)

VA =.Vco2 / FAco2
This alveolar ventilation equation provides an accurate
estimate of .VA using just spirometric testing and not requiring a blood sample. However.Vco2 is most often calculated under STPD conditions while .VA is usually reported in BTPS. Thus, a complete solution for .VA may necessitate converting between these volume measurements using the procedure outlined
in Chap. 1: (P1 · V1)/T1 = (P2 · V2)/T2.


Explain how the V(A) is calculated using the physiological dead space equation. Why are the two different equations useful?

First, V(D) is calculated and it is subtracted from V(E)

VD = [(Paco2 − P_E co2)/ Paco2] · VT

This physiological dead space equation yields a very
similar estimate of VD and
D as deduced from the alveolar
ventilation equation. The two mathematical approaches differ
mostly by the assumptions made and the types of patient
data needed to make the calculations: spirometric estimate of
end-tidal CO2 versus access to arterial blood gases. One is a
non-invasive technique only requiring awake subjects who can
respond to instructions to expire completely, etc. The other
can be done at the bedside of intubated, catheterized patients
irrespective of their cognitive status.


What is the normal anatomical dead space? Physiologic dead space? What about VD/VT? What causes it to decrease? Increase? What is the clinical result of increased VD/VT?

Anatomical VD is ~2 mL/kg of predicted body weight
(Chap. 4), with physiological VD equal to or only slightly
larger than anatomical VD in healthy lungs. The ratio of physiological
VD/ VT is 0.2-0.4 at rest, decreasing with increases in
VT in healthy adults who breathe more deeply during exercise.
A person’s VD/ VT increases with age, presumably due
to progressive respiratory muscle weakness, loss of alveolar
surface area, or fi brosis and may exceed 0.60 in individuals
with cardiopulmonary disease. This increased VD/ VT refl ects
worsening ventilation-perfusion mismatching or right-to-left
shunt (Table 8.1). As VD/ VT increases, the work of breathing
becomes excessive as patients struggle to overcome such
wasteful dead space ventilation (Chap. 6).


What is the alveolar gas equation? How is it used to solved for PAO2? What is (A-a)PO2? What assumptions are made in these equations/where are the non-variables derived?

PAo2 = PIo2 − (Paco2/R)

PIO2 is assumed to be 149mmHg.
PaCO2 is obtained from blood gases.
R is VCO2/VO2 and ranges from .7 to 1.0 but is often assumed to be 0.8.

(A-a) PO2 is simply PAO2-PaO2.

PaO2 is obtained from blood-gas measurements.