Circulatory shock remains a frequent, acute life-threatening condition with a high mortality, despite intensive treatment. Shock is often detected late, because circulatory disturbances in shock are clinically visible only to a limited extent. Clinical features, such as pallor, an increased pulse rate and, when detected, oliguria or anuria are barely specific. The diagnosis is usually made when there is a significant and persistent fall in the arterial blood pressure along with evidence of decreased tissue perfusion. The aim of the circulation is to deliver an adequate volume of oxygen at an adequate partial pressure to replace the oxygen used at the terminal oxidase of the respiratory chain in the mitochondria. This oxygen supply is vital, as 95% of the energy generated by the body normally originates from aerobic pathways, and as the entire oxygen store of the body would support resting needs for maximally 5 min (Kreuzer & Cain, 1985). Thus, inadequate tissue perfusion and impaired tissue oxygenation, possibly from maldistribution of the blood flow, are the common denominators of shock (Hardaway, 1969; Shoemaker, 1971, 1973; Shoemaker et al., 1971a, b, 1973; Bryan-Brown, 1978; Wilson, 1980; Hardaquay, 1981). However, direct measurement of tissue perfusion and/or oxygenation is still difficult.

Until now only systemic parameters such as arterial blood pressure, central venous pressure, pulmonary arterial blood pressure and cardiac output have been monitored. In shock these parameters are corrected meticulously, but the therapeutic interventions may actually impair tissue perfusion and tissue oxygenation. Attaining normal haemodynamic values may thus not be the optimal goal of treatment, since the compensatory bodily responses to stress also produce departures from the normal haemodynamic values (Shoemaker & Czer, 1979).