Affiliations: Department of Pharmacology
State University of Campinas
Campinas, São Paulo, Brazil ,
Medical Director, Hyperbaric Medicine
Associate Professor of Medicine
University of Utah Medical Center
Director of Research
Professor of Medicine
University of Utah Medical Center
Salt Lake City, UT
We read with interest the article entitled, “Venous and
Arterial Gas Embolism Associated with Positive Pressure
Ventilation,” by Weaver and Morris (April 1998).1 They
elegantly reported a case of massive gas embolism in a patient who died
after becoming hemodynamically unstable and sustaining a right
ventricular infarction. The development of right-heart failure and
circulatory shock secondary to a massive increase in pulmonary vascular
resistance requires prompt management, and any therapeutic attempt to
improve hemodynamics is of utmost importance.
Some recent experimental data consistently support the hypothesis
that inhaled nitric oxide might be a therapeutic option in the acute
management of pulmonary gas embolism.2,,3 For example, 3
ppm of inhaled nitric oxide attenuated the increase in pulmonary
vascular resistance and blunted the decrease of cardiac output after a
massive air embolism in dogs.2Similar effects were
observed when nitric oxide (3 or 40 ppm) was administered during a
venous air infusion in dogs.3In addition, although
controlled trials are needed to confirm the beneficial effects of
nitric oxide inhalation in patients with pulmonary
embolism,4some authors described significantly lower
pulmonary artery pressures and increases in cardiac output after nitric
oxide therapy during this critical condition.5 Even though
the relevance of these findings remains to be elucidated, we believe
that nitric oxide therapy could partially reverse the circulatory
collapse caused by a massive gas embolism.
Correspondence to: Jose Eduardo Tanus-Santos, MD, PhD,
Department of Pharmacology, Faculty of Medical Sciences, State
University of Campinas, 13081-970 Campinas, São Paulo, Brazil,
We agree with Drs. Tanus-Santos and Moreno that
the clinical relevance of these findings remains to be elucidated. The
experimental observations in dogs cannot be extrapolated to the sick
human. As Drs. Tanus-Santos and Moreno indicate, controlled trials are
needed. Such trials will likely depend upon the development of
methodology for early detection (eg, esophageal echo) and
its widespread dissemination in a large consortium of investigative
centers. The infrequent clinical recognition of massive air
embolism requires that a large number of investigative centers
participate. One would probably design an explicit, exportable method
to assure investigative uniformity among participants. Some would, we
suspect, rank this clinical problem below many others to which priority
might be given if the investment in an adequate multicenter consortium
Correspondence to: Lindell K. Weaver, MD, FCCP, Medical
Director, Hyperbaric Medicine, LDS Hospital, Eighth Avenue and C
Street, Salt Lake City, Utah 84143; e-mail: firstname.lastname@example.org
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