In Reply:
We thank Dr. Roth for the interest in our experimental study, in which we described the changes in blood flow and ventilation secondary to a controlled regional pulmonary vascular occlusion.1 These physiologic compensations likely occur through an increase in airway resistance (bronchoconstriction) in the nonperfused lung areas. As a result, ventilation of nonperfused alveoli is reduced, limiting the increase in dead space fraction and preserving the ventilation-perfusion matching. Bronchoconstriction, and therefore wheezing, are thus possible symptoms of pulmonary embolism2,3 and might (rarely) be so pronounced to be mistaken for severe asthma.4
Given these premises, Dr. Roth asks if bronchoconstriction (wheezing) secondary to pulmonary embolism should be treated, as an effective resolution of bronchoconstriction could cause an increase in dead space fraction, thus increasing the required minute ventilation to exhale the produced carbon dioxide load. Again, we thank him for the very interesting and clinically relevant question.
It is our opinion that, once pulmonary embolism is diagnosed (or highly suspected) in a wheezing patient, the choice whether to use bronchodilators should be made according to the specific clinical condition and keeping in mind the particular pathophysiology of bronchoconstriction.
For instance, in case of a patient with diffuse wheezing leading to severe air trapping, increased intrathoracic pressure and hemodynamic impairment, we think that pharmacologic bronchodilation might be a reasonable option in order to improve the associated hemodynamic derangement. In particular, it is reasonable to assume that such a patient would be intubated and mechanically ventilated. In this context, therefore, the need to increase mechanical ventilation due to the worsening ventilation-perfusion matching would not be of great concern, as the ventilator would carry out at least part of the additional work of breathing.
On the other hand, in case of a spontaneously breathing, hemodynamically stable patient, the treatment of bronchoconstriction might paradoxically increase, rather than decrease, the work of breathing, due to the increased dead space fraction. According to this pathophysiologic reasoning, in this setting, i.e., a condition likely caused by regional (not diffuse) bronchoconstriction, bronchodilators could therefore be used with caution, or even be avoided.
Overall, the treatment of pulmonary embolism should of course have the priority. Indeed, the restoration of blood flow to previously nonperfused lung regions will reestablish carbon dioxide delivery to the alveoli and in exhaled air, thus reverting hypocapnic bronchoconstriction and the ensuing wheezing.3
Competing Interests
Dr. Pesenti reports advisory board membership at Fresenius AG (Germany) and medical advisory board membership at Baxter (Italy). The other authors declare no competing interests.
