All studies examined in the Consensus Conference by Landoni and others share the common physiopathological background of maintaining adequate tissue oxygenation [3]. It is a well-known fact that surgery is associated with a systemic inflammatory response with increased oxygen consumption (VO₂). In high-risk surgical patients (expected mortality >5 %), whose characteristics are summarized in Table 6.2, the cardiovascular system cannot counterbalance this increased oxygen consumption with adequate delivery. The oxygen debt thus created plays a role in tissue hypoxia, which results in post-operative complications and, in some cases, death [13]. Specifically, in the intestine, reduced oxygen perfusion causes damage to the endothelial barrier with the release of endotoxins into blood circulation; these endotoxins activate and stimulate the multi-organic inflammatory response [4]. Hence, it is explained how maintenance of renal function and prevention of tissue hypoperfusion are strictly related to perioperative survival. Tissue hypoxia, at an early stage, is “hidden,” as it cannot be diagnosed through common clinical parameters such as mean arterial pressure, heart rate (HR), or central venous pressure. Even less useful are early clinical signs such as diuresis, state of consciousness, and peripheral perfusion. Prevention of tissue hypoxia depends on several factors and involves a balance between oxygen delivery and consumption (Fig. 6.1). While oxygen consumption can be only minimally modified, its delivery is the key element in hemodynamic optimization. It is given by the product of the following parameters:

DO₂ (mL/min) = cardiac output (CO) (L/min) × arterial oxygen content (CaO₂)

While you need to preserve arterial oxygen content by maintaining adequate hemoglobin and blood oxygen level, a key element of hemodynamic optimization is given by the CO or CI, as it can be rapidly monitored and adapted to the patient’s bedside. Different systems of hemodynamic monitoring (Table 6.3) allow, with different methods depending on their technology and invasiveness, to estimate the stroke volume (SV) and, from this, to obtain the cardiac output value (CO = SV × HR). Besides this perfusion index, current devices allow for a more precise and focused hemodynamic management through the measurement of other parameters: