Barotrauma vs Volutrauma

David C. Chao and David J. Scheinhorn

Chest 1996;109;1127-1128
DOI 10.1378/chest.109.4.1127

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1996 BY THE AMERICAN COLLEGE OF CHEST PHYSICIANS
 communications to the editor
Communications for this section will be published as space and
priorities permit. Thecomments should not exceed 350 words in ventilator Pao=45cmH20
length, with a maximum of five references; one figure or table can
be printed. Exceptions may occur under particular circumstances.
Contributions may include comments on articles published in this
periodical, or they may be reports of unique educational character.
Specific permission to publish should be cited in a covering letter or
appended as a postscript.

Barotrauma vs Volutrauma
Pes
=0cmH2O
To the Editor: (atm)
The barotrauma vs volutrauma debate continues, but the vo¬
lutrauma camp seems to have gotten the upper hand. A statement
in a contemporary textbook1 on mechanical ventilation declared, "It
is clear that microvascular lung injury and pulmonary edema dur¬
ing mechanical ventilation are the consequences, not of 'barotrau¬
ma,' but, rather, of Volutrauma.' We would caution both camps
"

Pao=0 (atm)
that while vindication is sweet, a change in perspective may bring
insight to the phenomenon of ventilation-induced injury.
The studies23 that brought steam to the volutrauma camp suffer
from a flawed presumption. First, the researchers demonstrated
that lung injury developed in animals ventilated at high pressure/
high tidal volume. They simulated high pressure/low volume ven¬
tilation by thoracoabdominal strapping and found no injury in this
group, concluding that high pressure per se did not cause injury.
They3 then simulated high volume/low pressure ventilation using an
iron lung to achieve lung overdistension and found injury.proving Pes
high volume to be the culprit. Unfortunately, the studies fail to =-45cmH20
consider alveolar pressure from the proper reference pressure.
Figure 1 shows the relevant pressures at end-inspiration in the
experiments. In Figure 1, Top, high inspiratory pressure hyperin-
flates the lung, resulting in injury. In Figure 1, Center, the iron lung
creates a large negative pressure at chest surface (Pes) hyperinflat-
ing the lung while maintaining alveolar pressure (Palv) at 0. How¬
ever, the distending pressure of the respiratory system
(Prs=Palv-Pes) is exactly the same as in Figure 1, Top. The
distending pressure of the lung (Palv-Ppl) is also identical. In Fig¬ ventilator Pao=45cmH20
ure 1, Bottom, the chest/abdomen is not allowed to expand. This
results in very high airway opening pressure (Pao), Palv, Ppl, and
Pes, but the transpulmonary pressure (Palv-Ppl) remains low.
Furthermore, the "stretch" in the alveoli is caused by the tensile
stress in the alveolar wall produced by the distending pressure.
Laplace's law states thatwall stress a is proportional to P (transmural
pressure) times the diameter. Transmural pressure and diameter of
the alveoli have equal roles in wall stress. In Figure 1, Top and
Center, the transmural pressures and alveolar sizes are the same,
thus the wall stresses are identical. In fact, this is how the
researchers can achieve similarly high tidal volumes without a Pcs=35cmH20
change in lung compliance. Therefore, these studies have not really
dissected the respective effects of pressure and volume, but they
merely created an "illusion" of a low pressure situation as shown in
Figure 1, Center, and high pressure as in Figure 1, Bottom.
Properly referencing one's pressure measurements is of utmost W///////^^^^^
importance, lest we arrive at misguided conclusion. For example, Figure 1. Top: High-pressure/highVolume. Center: Negative-pressure/
when a diver at a 66-foot depth is breathing at more than 2,000 cm high volume (iron lung). Bottom: High-pressure/low volume.
CHEST/109/4/APRIL, 1996 1127
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1996 BY THE AMERICAN COLLEGE OF CHEST PHYSICIANS
H2O, we'd be surprised not to find lung injury unless we realize that
the ambient pressure exerted on the chest wall (Pes) is also 2
atmospheres, and transpulmonary pressure remains normal (anal¬
ogous to Figure 1, Bottom). Likewise, a thin inner tube of a tire can
withstand the weight of a car because the rigid outer tube limits its
transmural pressure, thus keeping the wall stress low.
Undoubtedly, epithelial damage and pulmonary edema occur
when alveoli are overstretched. However, the overstretching (vo¬
lutrauma) results directly from distending pressure (barotrauma).
There can be no strain without stress, and emerging data show that
high wall stress has a pathogenic property, as expected.4 We pro¬
pose to keep the term "barotrauma" in referring to extra-alveolar air,
and to use the more accurate term "alveolar stress injury" for the
phenomenon of stress/strain induced epithelial/endothelial dam¬
age. It is time that we analyze ventilator-induced lung injury using
principles of physics and reconcile the barotrauma and volutrauma
camps.
David C. Chao, MD, FCCP, and
David J. Scheinhorn, MD, FCCP,
Barlow Respiratory Research Center,
Los Angeles
REFERENCES
1 Dreyfuss D, Saumon G. Ventilator-induced injury. In: Tobin MJ,
ed. Mechanical ventilation. New York: McGraw-Hill, 1994; 808
2 Carlton DP, Cummings JJ, Scheerer RG, et al. Lung overexpan-
sion increases pulmonary microvascular protein permeability in
young lambs. J Appl Physiol 1990; 69:577-83
3 Dreyfuss D, Soler P, Basset G, et al. High inflation pressure pul¬
monary edema: respective effects of high airway pressure, high
tidal volume, and positive end-expiratory pressure. Am Rev
Respir Dis 1988; 137:1159-64
4 West JB, Tsukimoto K, Matieu-Costello O, et al. Stress failure in
pulmonary capillaries. J Appl Physiol 1991; 70:1731-42
Propofol for ICU Sedation
To the Editor:
I read with pleasure the excellent review by Mirenda and Broyles
(1995; 108:539-48) in a recent issue of CHEST regarding propofol
for ICU sedation. The article was comprehensive and generally well
balanced and should serve as a valuable resource to physicians in¬
volved in the ICU.
As a cardiac anesthesiologist with ICU responsibilities, I have
considerable experience with propofol infusion techniques. Clearly,
this drug represents a tremendous advance in anesthesia and seda¬
tion due to its pharmacokinetic profile. I believe the cost data from
Mirenda and Broyles are misleading. Table 5 on page 546 (CHEST
1995; 108:539-48) describes an overstated dose and therefore cost
of propofol for ICU sedation. According to their table, in a 70 kg
patient, 100 to 200 mg/h is a typical low dose. This would equal 24
to 48 pg/kg/min. This is accurate. However, the authors describe a
high dose of 500 to 1,000 mg/h, which equals 120 to 240 pg/kg/min.
These are dosages typically used for general anesthesia in the op¬
erating room. Indeed, the 240 dose is more than I have ever used.
Based on my hospital's acquisition cost of $0.48 per mL, a 70-kg
patient would use $92.16 at 20 pg'kg/min, $241.92 at 50 pg/kg/min,
and $483.84 at 100 pg/kg'min, still in the middle of the midazolam
range in Table 5 by Mirenda and Broyles. In most cases, if more than
100 pg/kg/min is needed, a small dose ofanother drug, perhaps even
a neuromuscular blocker, would be more suitable as well as cost-
effective.
1128
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1996 BY THE AMERICAN COLLEGE OF CHEST PHYSICIANS
Finally, I agree with the comments by Mirenda in his letter in
Critical Care Medicine1 that the most practical use of propofol is to
attain specific, short-term sedative goals in select patients. However,
I disagree with his statement that the "cost of propofol is three to
four times that of comparable doses of midazolam," and this is in¬
consistent with his own data.
Elden Sherman, MD,
Roper Hospital,
Charleston, South Carolina
Reference
1 Mirenda J. Letter to the editor. Crit Care Med 1995; 23:1304
To the Editor:
We appreciate the interest and concern of Dr. Sherman regard¬
ing propofol for ICU sedation (CHEST 1995; 108:539-48). We also
welcome the opportunity to clarify the issues raised.
The concerns over dosage ranges mentioned by Dr. Sherman are
obvious and noted repeatedly in the review. Table 1, in fact, thor¬
oughly describes recommended dosage guidelines for propofol use
in the ICU setting and concludes with the warning that long-term
use should attempt to be limited at 50 pg/kg/min. This goal is usu¬
ally not difficult to attain in the cardiac surgical ICU patient, though,
unfortunately, it may need to be exceeded in medical or trauma
patients, patients with relative contraindications to neuromuscular
blockade, or those patients exhibiting tolerance to ongoing sedation.
Though we certainly do not recommend dosages of 120 to 240 pg/
kg/min for long-term sedation in any ICU patient (nor does the
manufacturer), the point of including such (referenced) dosages in
Table 5 is to emphasize the possibility of a number of side effects
seen with such dosages; one side effect being a significant pharmacy
cost. As mentioned in the review, the physician who finds himself
prescribing such high doses should review the particular sedation
goals in his patient and adjust infusion rates using appropriate ad¬
juncts.
The issue of pharmacy cost of propofol is an important one,
though one that is often difficult to address due to variations in ac¬
quisition cost both geographically and chronologically. In an effort
to remain unbiased, Table 5, which lists typical pharmacy costs for
sedation, is referenced12 and based on the most recent data avail¬
able at the time of writing. Though the acquisition cost and meth¬
ods used by those authors may be different than that used by Dr.
Sherman, our own acquisition cost leads us to similar cost/24 h for
midazolam as stated in Table 5 as well as the "high dosage" of pro¬
pofol. As Dr. Sherman has shown, it is worthwhile for practitioners
to arrive at their own data based on cost at their particular institu¬
tions.
Finally, we should emphasize that our goal in writing the review
was to present the most recent data on propofol sedation in the ICU
to the ICU practitioner as objectively as possible. Unfortunately,
objective data on cost-benefit analysis are difficult to find. The study
by Carrasco et al,3 which found that the pharmacy cost of propofol
was consistently three to four times that of midazolam, was under¬
taken at one particular institution (in Spain), during a finite period
of time and by certain methods. These data may or may not
extrapolate to any one particular institution or practice pattern. As
such, we would hope that more objective data are generated, how¬
ever difficult or complex, concerning the cost-effectiveness of pro¬
pofol, or other sedatives, when used in the ICU.
Joseph V. Mirenda, MD,
Department of Anesthesiology,
Roanoke Memorial Hospitals; and
Gregory Broyles, RPh,
Communications to the Editor
 Barotrauma vs Volutrauma
David C. Chao and David J. Scheinhorn
Chest 1996;109; 1127-1128
DOI 10.1378/chest.109.4.1127
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1996 BY THE AMERICAN COLLEGE OF CHEST PHYSICIANS