Wasted Ventilation
Dead Space
• dead space is the volume of air which is inhaled that
does not take part in the gas exchange, either because
it (1) remains in the conducting airways, or (2) reaches
alveoli that are not perfused or poorly perfused. In
other words, not all the air in each breath is available
for the exchange of oxygen and carbon dioxide.
• About a third of every resting breath has no change in
O2 and CO2 levels. In adults, it is usually in the range of
150 mL.
• The total dead space (also known as physiological
dead space) is the sum of the anatomical dead space
plus the alveolar dead space.
Anatomical dead space
• Anatomical dead space is that portion of the
airways (such as the mouth and trachea) which
conducts gas to the alveoli.
• No gas exchange is possible in these spaces. In
healthy lungs the alveolar dead space is small;
measured by a nitrogen washout technique.
• The normal value for dead space volume (in ml) is
approximately the lean mass of the body (in
pounds), and averages about a third of the
resting tidal volume (450-500 mL).
Alveolar dead space
• Alveolar dead space is sum of the volumes of those alveoli which have
little or no blood flowing through their adjacent pulmonary capillaries, i.e.,
alveoli that are ventilated but not perfused, and where, as a result, no gas
exchange can occur Alveolar dead space is negligible in healthy
individuals, but can increase dramatically in some lung diseases due to
ventilation-perfusion mismatch.
• Calculating the dead space
• Just as dead space wastes a fraction of the inhaled breath, dead space
dilutes alveolar air during exhalation. By quantifying this dilution it is
possible to measure anatomical and alveolar dead space, employing the
concept of mass balance, as expressed by Bohr equation.
• where is the dead space volume and is the tidal volume;
• is the partial pressure of carbon dioxide in the arterial blood, and
• is the partial pressure of carbon dioxide in the expired (exhaled) air.
Physiologic dead space
• The concentration of carbon dioxide (CO2) in healthy alveoli
is known - it is equal to its concentration in blood since CO2
rapidly equilibrates across the alveolar-capillary membrane.
The quantity of CO2 exhaled from the healthy alveoli will be
diluted by the air in the conducting airways, and by air from
alveoli that are poorly perfused. This dilution factor can be
calculated once the CO2 in the exhaled breath is
determined (either by electronically monitoring the
exhaled breath or by collecting the exhaled breath in a gas
impermeant bag - a Douglas bag - and then measuring the
mixed gas in the collection bag). Algebraically, this dilution
factor will give us the physiologic dead space as calculated
by the Bohr equation:
Alveolar dead space
•
When the poorly perfused alveoli empty at the same rate as the normal alveoli, it
is possible to measure the alveolar dead space. In this case, the end-tidal sample
of gas (measured by capnography) contains CO2 at a concentration that is less than
that found in the normal alveoli (i.e. in the blood):
•
•
Caution: The end tidal CO2 concentration may not be a well defined number.
Poorly ventilated alveoli do not generally empty at the same rate as healthy
alveoli. Particularly in emphysematous lungs, diseased alveoli empty slowly, and so
the CO2 concentration of the exhaled air increases progressively throughout the
expiration.[
Monitoring alveolar dead space during a surgical operation is a sensitive and
important tool in monitoring airway function.[11]
During strenuous exercise, CO2 will rise throughout the exhalation and may not be
easily matched to a blood gas determination, which led to serious errors of
interpretation early in the history of dead space determinations.[8]
Example: For a tidal volume of 500 mL, an arterial carbon dioxide of 42 mmHg,
and an end-expired carbon dioxide of 40 mmHg:
and so
•
•
•
•
BEWARE OF TACHYPNEA WITH SMALL
TIDAL VOLUMES
• Clearance of carbon dioxide is determined by the alveolar
ventilation and the physiologic dead space.
• Residents frequently ask me: "why is this patient's PaCO2
(partial pressure of Carbon Dioxide in the blood) so high
when he has a minute ventilation of 30 liters per minute?"
• This is a common trap to fall into: confusing alveolar
ventilation (which is difficult to measure) with minute
ventilation (which is always measured). The difference
between the two is determined by the anatomical dead
space.
• Two patients have a minute ventilation of 10 liters/minute:
– Patient B is taking 50 breaths of 200ml tidal volume.
– Patient A is taking 20 breaths of 500ml tidal volume.
BEWARE OF TACHYPNEA WITH SMALL
TIDAL VOLUMES
• Using misplaced logic one would think that each would
have the same PaCO2. In fact patient B has a significant
respiratory acidosis, and patient A has a normal blood gas.
Anatomical dead space is approximately 150ml in an adult
male. It is important to calculate out the dead-space
(Vd/Vt) to tidal volume ratio for each patient: patient A has
a Vd/Vt of less than 30% (normal is 30%). Patient B has a
Vd/Vt of 75%.
What does this mean?
In the case of patient B, 75% of his respiratory effort is
being wasted, leading to severe muscular fatigue and
acidosis.
BEWARE OF TACHYPNEA WITH SMALL
TIDAL VOLUMES
• It is also important to realize that patients may have large amounts
of alveolar dead space: a patient can be receiving tidal volumes of
500ml and still have a dead space ratio of 75%: how?
Alveolar dead space is caused by increased volume of zone 1 (zone
1 is where alveolar pressure exceeds the perfusion pressure to the
lung unit: alveoli are ventilated but not perfused):
• Hypoperfusion - low pulmonary blood volume-pressure leads to
underperfusion of non dependent lung segments.
• Overdistension of compliant lung units: often caused by excessive
PEEP.
• Dead space is calculated by measuring the ratio of end tidal CO2
(etCO2) to arterial CO2 (PaCO2), using the equation:
• Vd/Vt = PaCO2 - PetCO2/PaCO2
BEWARE OF TACHYPNEA WITH SMALL
TIDAL VOLUMES
• It is important that you are aware of physiologic dead
space (anatomical dead space plus alveolar dead
space) in the modern setting of low tidal volume
ventilation for acute lung injury
• Using tidal volumes of 4 - 5ml/kg in patients with
significant atelectasis leads to considerable wasted
ventilation: as a result a much higher respiratory rate
than normal is required (25 to 30, frequently more) to
control PaCO2. This frequently leads to problems with
auto-PEEP
• We know that permissive hypercapnia is associated
with few complications, so most physicians elect to
allow the PaCO2to climb rather than compromising
oxygenation.