The cardiovascular system plays a key role in complex living organisms since it provides supplies for maintaining vital functions and, contemporaneously, gets rid of waste materials. It is formed by highly specialized subsystems that interact with each other to accomplish tasks (e.g. the optimization of arterial and pulmonary circulation) and even compete for resources as in, for example, the maintenance of the cerebral circulation during a massive haemorrhage. Subsystems have their own local regulatory mechanisms (e.g. mechanisms regulating blood flow in proximal microvascular districts) that interact with central neural commands reflecting the activity of the vasomotor and respiratory autonomous oscillators, with reflex neural commands occurring in response to changes in some controlled variables (e.g. arterial pressure) and with humoral factors. All these regulatory mechanisms act rhythmically, producing incessant adjustments in cardiovascular variables visible from beat-to-beat recordings. These variations are referred to as 'cardiovascular variability' and occur over a wide frequency range including very slow rhythms (e.g. ultradian periodicities) and oscillations even faster than heart rate. The magnitude of these variations depends on the gross amount of the activities of the autonomous central oscillators, on the resonance of the closed-loop mechanisms, on the gain of the relationship between variables and on the possibility that a network of distributed oscillators with negligible activities becomes entrained or remains sparse.The presence of multiple regulatory mechanisms contemporaneously active over different time scales and capable of varying over time the relationships among variables generates the dynamic complexity of cardiovascular variables. This complexity also depends on the presence of mechanisms favouring synchronization among the activities of subsystems according to n : m coupling ratios (i.e. n cycles of activity of one subsystem correspond to m cycles of the other), thus reducing dimensionality of the cardiovascular system, and on the amount of information exchanged among subsystems (i.e. on their degree of isolation).Current evidence suggests that the assessment of the complexity of cardiovascular regulation could provide important information about the underlying regulatory mechanisms. In particular, it has been shown that a modification of complexity indices, resulting from depressed organ function, a loss of interaction among subsystems, an overwhelming action of a subsystem over others and an impairment of regulatory mechanisms, is a clear hallmark of a pathological situation. Interestingly, since the complexity of cardiovascular regulation can be evaluated from variables that are routinely and non-invasively estimated during the most common medical examinations, this assessment does not require additional procedures and devices. On the contrary, it necessitates