In this issue of the Journal of Clinical Monitoring andComputing, Dr. Vistisen and colleagues emphasise theinadequacy of the variation in the pre-ejection period (PEP)following deep breathing to predict the hemodynamicresponse to controlled haemorrhage [1]. The present clin-ical report may lead to the implication that this marker ofhypovolemia should be disregarded in cases of spontaneousventilation.The PEP includes excitation–contraction coupling andisovolumic contraction. Accordingly, the normovolemic leftventricle has a short PEP, whereas a hypovolemic ventriclehasalongPEP.Inthisregard,mechanistically,searching thepreload prediction from the pre-ejection period measure-ment makes sense. Indeed, there have been numerous pub-lished studies, both in human patients and in various animalmodels supporting the use of the pre-ejection period tocharacterise the preload [2]. These findings are based ondirect observations and are independent of the type of res-piration, as studies have been performed under conditions ofspontaneous [3] and mechanical ventilation [4, 5].With this in mind, it is rather surprising that little workhas been done to measure the reliability of these systolictime intervals during deep inspiration and/or the Mullermanoeuvre [6]. The article by Vistisen et al. addresses thisissue by presuming that through its impact on the respira-tory change in PEP (DPEP), a deep breathing manoeuvrecould be a preload varying method useful for predicting themagnitude of change in the cardiac output (CO) followingblood donation in healthy volunteers. Interestingly, it mightseem strange that the authors found that it was impossibleto demonstrate such a predictive value. So far, thehypothesised underlying physiology was confirmed, aswhatever the deep breathing frequency (0.1 vs. 0.167 Hz),the manoeuvre induces characteristic fluctuations in thePEP pattern. However, the authors demonstrated thatbecause the PEP is a parameter that is strongly dependenton heart rate variability (HRV), the DPEP also depends onthe respiratory induced HRV (RMSSD).On a first reading, there are several open questionsarising from the study of Dr. Vistisen et al.; perhaps themost important is the reason why the cyclic change in thePEP (DPEP) was not able to predict the stroke volumeresponses to controlled haemorrhage. Indeed, it might seemstrange that at the same time, the authors demonstrate thatwhatever the deep breathing frequency (0.1 vs. 0.167 Hz),this manoeuvre induces significant characteristic fluctua-tions in the PEP values. Although, we may speculate that anoisy pulse plethysmographic signal may make an accurateassessment of the DPEP difficult [7]; in this regard themethodology used by the authors is perfect.In principle, the absence of the clinical relevance ofcyclic changes in the PEP while the same parameter issensitive to a deep inspiratory manoeuvre may result fromthe influence of the expiratory phase on the PEP mea-surements [8]. Indeed, a forced inspiratory manoeuvre maybe followed by a forced expiratory effort that increases theleft-ventricular afterload through an increase in theabdominal pressure. Taking everything into consideration,
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Jun 1, 2016
B Herrero Cortina + 7
Open Access
