To the Editor:
The article by Volpicelli et al.1 aimed to assess the possible role of B-lines by lung ultrasound (LUS) alone or in combination with left ventricular ejection fraction (LVEF) in predicting high or low levels of pulmonary artery occlusion pressure (PAOP) and extravascular lung water (EVLW). The multicenter study comprises the evaluation of critically ill patients from different clinical settings and conditions predisposing to hemodynamic instability. Notwithstanding these valuable aspects, the study in our view did not add any useful information on the role of LUS in the clinical management of these patients. Data indeed appear to fail in demonstrating any usefulness of A- and B-patterns alone in detecting high PAOP, as sensitivity and specificity of these methods achieve considerable values only when LVEF, a widely recognized and used index of cardiac performance, is added to the model. As per authors’ conclusions, “only the combination of the A-pattern at LUS and the normal LVEF estimated by focused cardiac ultrasound reliably indicates low PAOP,” meaning that this point represents the most important finding of the study. In this context, it is our opinion that many issues need to be addressed. The authors did not clearly state why LVEF was used, namely the rationale of combining LUS findings with a measure of systolic function. Considering the variety of clinical conditions reported, LVEF cannot indeed be supposed to be affected in any case and is therefore neither a valuable nor a sensitive predictor of hemodynamic instability in any given patient. This consideration also leads us to underline the need of including LVEF data in the article, as well as of detailing the conditions of patients whose evaluation of LVEF and LUS pattern was associated with high predictive values for PAOP assessment. The absence of any improvement of accuracy in predicting EVLW by combining LVEF and A-pattern further supports the hypothesis that LVEF cannot be chosen as a target tool to assess hemodynamic state in the particular population studied.
As far as LUS findings, the article did not accurately describe how patients were studied (supine or seated position), the clinical setting (dyspneic patients?), potentially increasing the detection of LUS artifacts,2 as well as the possible underlying mechanisms. Indeed, the authors did not provide any explanations on possible related mechanisms associated with the high prevalence of A-pattern and high PAOP in chronic heart disease patients, whereas B-pattern was mostly found in combination with high PAOP in patients with normal cardiac function (mostly sepsis and pulmonary failure).1 Is the study showing that lung fluid is increased in the setting of sepsis and acute pulmonary failure regardless of the underlying disease? If this is the case, which are the EVLW values in this group of patients? Also, which kind of interstitial syndrome, whose detection through B-lines is advocated throughout the article, are the authors referring to in the study, and particularly in this patient group?1
With no answers to these questions, we wonder how the conclusion of using LUS in the first approach of patients requiring fluid resuscitation could be driven by the present data.
We therefore claim the need for emphasizing the useful but limited power of LUS in the evaluation of critically ill patients,2 having no study been performed to actually validate the aforementioned ultrasound signs as pathophysiologically associated with any of the disease causing hemodynamic instability.
The authors declare no competing interests.