Intravenous administration of fluid is among the most common in-hospital procedures and it is argued that for supine persons normovolaemia is defined by the maximal stroke volume of the heart or cardiac output. As administration of fluid, however, means that haematocit decreases and therefore cardiac out increases, a definition of normovolaemia based on the maximal venous oxygen saturation is more operative and, in fact, it is venous oxygen saturation rather than cardiac output that is regulated. Also, fluid administration is guided by recording of heart rate and blood pressure. Because blood pressure is defended by arterial baroreceptors, it is kept constant until the central blood volume is reduced by ~30%. At that stage a Bezold-Jarish-like reflex is elicited and vasodilatation to skeletal muscles means that total peripheral resistance reduces blood pressure and vagal stimulation reduces heart rate eventually to zero. Paradoxically, the patient is pale due to elevated plasma vasopressin. The reduction in heart rate is attenuated if trauma involves pain and, equally, static exercise may be used to combat development of a vaso-vagal syncope. Only if the patient surveys that stage of hypovolaemia is the traditional described tachycaridia (heart rate > 100 bpm) of shock manifest and approximately 30% of patients die despite intensive care medicine in what may be considered a parallel to the experimentally induced irreversible shock. It is advocated that the description of normovelaemia becomes central in the physiological description of the circulation so as to make management of the circulation as accurate as handling of ventilation.