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The measurements were performed in duplicate, first before volume expansion and then 30 min after volume expansion using 500 ml 6% hydroxyethyl starch (HES) (130/0.4). Ventilatory settings and dosages of inotropic and vasopressor drugs were held constant. check details All patients were maintained in the 30�� head-up position for the duration of the study while hemodynamic measurements were being taken since it has been shown that body position may influence SVV measurements.[12] Apart from these hemodynamic data, we also recorded the cause of sepsis (i.e., bacterial pneumonia, abdominal sepsis, meningitis, etc.), number of patients with or without vasopressor support, underlying disease conditions such as, chronic obstructive pulmonary disease (COPD), diabetes mellitus (DM), ischemic cardiomyopathy, peripheral vascular disease (PVD), and chronic renal failure (CRF), as well as the results of any echocardiography, if performed. The number of patients surviving their stay in the CCU was also recorded. Therapeutic protocol The therapeutic protocol is shown in Figure 1. All patients were sedated and mechanically ventilated in a volume-controlled mode with the tuclazepam tidal volume of 8 ml/kg since the tidal volume can significantly affect the SVV value, and an inspiratory/expiratory ratio of 1:2. The level of positive end-expiratory pressure was recorded for each patient. Spontaneous breathing activity was looked for by visual inspection of the airway pressure curve. To ensure that the respiratory changes in SVV measurement reflected only the effects of positive pressure ventilation, patients Tofacitinib mouse were sedated or paralyzed if detected to have spontaneous breathing activity. Patients were divided into two groups, according to the percent increase in CI, in response to volume expansion. We assumed that a 15% change in CI was needed for clinical significance according to previous studies.[13,14] Therefore, patients with a CI increase induced by VE >15% and