Our study demonstrates that alterations in StO2-derived parameters were predictive of extubation failure after a clinically successful SBT.
To our knowledge, this is the first study showing that regional oxygenation parameters are associated with extubation outcome. The peripheral circulation has been previously studied in the setting of a cardiovascular stress test such as the SBT. Several studies showed that changes in gastric mucosal pH within the SBT were predictive of the clinical outcome of such SBT [12,13,14,15]. Similar results were obtained when assessing the peripheral circulation by means of NIRS, non-invasively monitoring oxygenation of the skeletal muscle within the SBT [16, 22, 23]. However, they were all small studies, and never explored the ability to predict the outcome of the overall weaning process. In this prospective study, we analyzed the utility of StO2-derived parameters in the extubation process, after a clinically successful SBT. Our results add new evidence on the usefulness of regional non-invasive parameters as a complimentary tool in monitoring the cardiovascular performance of critically ill patients. Indeed, our data suggest that the inclusion of StO2 monitoring in the weaning process might help prevent failed extubations, and therefore, the potential negative consequences on the outcome of critically ill patients.
Transitioning from positive pressure ventilation to spontaneous ventilation determines an increase in the work of breathing, and thus, an increase in the oxygen demand of the respiratory muscles. Such increase in the metabolic demand causes a sympathetic activation, in an attempt to optimize cardiac output delivery to the metabolically active tissues [24], and to increase vasomotor tone, redistributing blood flow away from the periphery toward the respiratory muscles [10, 25]. The ability of the cardiovascular system to meet this increased demand might be closely related to the ability of the patient to tolerate spontaneously breathing. Therefore, when the cardiovascular performance is limited, and/or the cost of breathing excessive, extubation failure will be more likely to occur. In these situations, the increase in sympathetic tone might be more accentuated, as the cardiovascular system continues to attempt to match cardiac output to an increasing metabolic demand. Indeed, clinical criteria for determining the success of the SBT are essential symptoms of excessive sympathetic activity (i.e., tachycardia, hypertension, agitation). A subclinical manifestation of the sympathetic activation would be the degree of peripheral vasoconstriction and/or the increase in the metabolic rate, and this is the basis for regional oxygenation measurements with NIRS.
Increased local oxygen extraction rate
Our data confirmed that relative increases in DeO2 during a 30-min SBT are associated with extubation failure, independent of other respiratory and hemodynamic parameters. The observed increases in DeO2 within the SBT might be explained by two different, but potentially concurrent, pathophysiological mechanisms: (1) local supply–demand dependency in low or inadequate blood flow states, such as blood flow diversion from the periphery; and (2) increase in local metabolic rate.
The increase in oxygen demand of the respiratory muscles during an SBT may lead to blood flow redistribution via activation of the sympathetic–adrenal system. When accentuated, this compensatory mechanism might cause a stealing effect from the periphery [10]. Accordingly, one would expect decreases in blood content of the sensed area [19, 26], along with relative increases in the DeO2 rate (either due to the decreased Hb content or to the sympathetically driven increase in the metabolic rate). In our population, extubation failure was associated with significant increases in DeO2, but no change in THI. Conversely, the success group showed no change in DeO2, with significant increases in THI. Such observations suggest that cardiac output increased in those patients who succeeded the weaning process. In those patients who failed, since we did not measure stroke volume, the interpretation of the lack of changes in THI is more complex. In a model of simulated hypovolemia, Bartels et al. reported that THI measured on the thenar eminence detected slight decreases in stroke volume, but changes were minimal, as compared to measurements on the forearm [26]. Therefore, we cannot exclude some degree of stealing effect as results of a limited sensitivity of the technology. Finally, a balanced effect of increased cardiac output and peripheral vasoconstriction, resulting in no changes in THI, cannot be excluded.
NirVO2, an estimation of local oxygen consumption [20, 21], increased in both groups during the SBT, but the magnitude of this increase was significantly higher in the extubation failure group. NirVO2 differences might reflect dissimilar degrees in sympathetic activation in the setting of inadequate cardiovascular response. This hypothesis is supported by studies that showed significant increases in plasma catecholamines during the SBT, especially in patients who failed an SBT [27, 28]. Overall, our data suggest that the increase in DeO2 in the extubation failure group might be mainly related to an increase in local oxygen consumption, although some degree of blood flow diversion cannot be ruled out.
Local hyperemic response after transient ischemia
We also observed that baseline endothelial performance, as measured by the StO2 hyperemic response, was independently associated with extubation outcome. Our findings on the predictive value of the StO2 hyperemic response are not surprising. Activation of the sympathetic nervous system is a major component of the neurohumoral response to the increased oxygen cost of breathing. Catecholamine release mediates vasoconstriction of peripheral vascular beds, and also, via ß-adrenoceptors, promotes vasodilation of the coronary arteries, and improves contractility. The functional impairment of the endothelium has been associated not only with poor peripheral response, but also with diminished ß-adrenoceptor sensitivity, limiting the cardiac response [29]. Therefore, endothelial dysfunction might be a potential marker of the ability of the patient to respond to the hemodynamic changes produced by the discontinuation of ventilatory support. According to our observations, we might hypothesize that vascular endothelial integrity, evaluated in peripheral skeletal muscle, might be relevant when facing a cardiovascular stress test such as transitioning from MV to spontaneously breathing.
Study limitations
Our study has relevant limitations. First, it was carried out in a single center. Albeit we expect that similar patients should behave similarly, weaning approaches may vary across centers affecting the predictive value of these StO2-derived parameters. Thus, this study needs to be duplicated across other centers. Second, we did not determine the cause of weaning failure in patients who were considered to fail. We merely identified that they did fail. We can expect different behaviors of StO2 parameters in patients who fail because of limited cardiovascular reserve from patients who fail because of upper airway obstruction and/or impaired secretions’ management. This issue must be taken into account in future studies. Finally, we studied a heterogeneous ICU population. Since the observed predictive value of StO2 might vary across populations, further studies including selected homogeneous critically ill patients are required.