hemodynamics and energy failure

Adequate hemodynamics not only means adequate blood flow and arterial pressure values but also an oxygen supply necessary to properly answer to biological needs. Proper oxygenation is synonymous of proper energy supply. Energy failure is a life threatening condition that can be due not only to hemodynamic insufficiency but also to mitochondrial impairment or a combination of the two. Challenge tests are available to assess the origin of energy failure, i.e. volume load and dobutamine test. If the response to this tests is an increased oxygen consumption and a decrease of lactate and its correlates due to an increased oxygen transport the mitochondrial function is still adequate. If oxygen consumption does not increase mitochondrial function is impaired due to a direct insult or long-lasting hypoxia. It appears quite clear that an aggressive hemodynamic treatment is useless in case of mitochondrial dysfunction. Moreover long-lasting energy failure may lead to mitochondrial disfunction of secondary origin. According to the observation that patients with higher mean CI, DO2 and VO2 had better outcome, “supra-normal hemodynamic values” became the target of several studies and of the treatment of intensive care patients. Hoewever Hayes et al. found that the mortality of patients targeted on “supra-normal values” presented higher mortality, while Gattinoni et al found that patients targeted to obtain supra-normal hemodynamic values, normal values or SVO2 >70% had the same mortality. On the contrary Rivers et al, 10 years later the study of Gattinoni, found that septic patients targeted to SvO2 > 70% had a better outcome than the ones treated to have an adequate arterial pressure. The possible reasons of these discrepancies may be due to the different times of intervention. It is possible, in fact, that in critically ill patients short times of intervention may solve the energy failure avoiding mitochondrial impairment. Analyzing the different studies, Shoemaker enrolled peri-operative patients, Rivers enrolled patients in emergency room 2 hours before the intensive care unit (ICU) entry, while Gattinoni’s study analyzed a general ICU population (up to 72 hours). It is then conceivable that the positive results found by Shoemaker and Rivers were not found by Gattinoni. Accordingly a meta-analysis by Kern and Shoemaker pointed out that only rapid interventions may reduce mortality. On this wavelength are even the Surviving Sepsis Campaign guidelines that suggest within the first 6 hours of treatment: central venous pressure within 8-12 mmH, mean arterial pressure higher than 65 mmHg, urinary output higher than 0.5 ml/kg/hr, ScvO2 >65% or SvO2 > 70%. In conclusion, time is essential as an early treatment of hemodynamic failure is likely associated with improved survival, before an irreversible mitochondrial damage