2,833 publications from this institution
Data on the risks and benefits of blood transfusion are conflicting, and with recent changes in blood transfusion practice, including the widespread introduction of leukoreduction, it is time to reevaluate our transfusion triggers.
Low cardiac output in acute heart failure can result in a functional impairment of organs, when tissue hypoxia occurs and cardiogenic shock develops. To restore cardiac output, various forms of therapy can be considered. Fluid replacement is sometimes beneficial in acute situations where oedema can reduce effective plasma volume. Vasodilators are often contra-indicated in shock, when arterial pressure is usually low. Inotropic therapy consists primarily of the administration of adrenergic agents. Dopamine and noradrenaline can be indicated in severe hypotension, to maintain coronary perfusion. Dobutamine is the catecholamine of choice to increase myocardial contractility. However, decreased responsiveness of the myocardial receptors to adrenergic stimulation rapidly becomes an important limitation. Phosphodiesterase inhibitors represent an interesting option to increase contractility, also by increasing cyclic AMP levels in the myocardium. In this respect, the combination of phosphodiesterase inhibitors with adrenergic agents is attractive. The additional vasodilatory properties of these agents can contribute to the increase in cardiac output with limited risk of further reduction in arterial pressure. In 13 patients with cardiogenic shock persisting despite the use of adrenergic agents, the addition of enoximone, 0.5 mg/kg, resulted in significant increases in cardiac index and stroke volume index and a significant decrease in pulmonary artery balloon occlusion pressure without consistent change in mean arterial pressure. In 8 patients, a second infusion of 0.5 g/kg amplified these effects. All but one of these patients survived the episode of cardiogenic shock, and 5 patients were discharged alive. In some cases, even lower doses of enoximone resulted in dramatic increases in cardiac output and oxygen transport in patients already treated with dobutamine with limited success.
Our study documents a direct relationship between the serum lactate level on ICU admission and not only the risk of death in ICU but also the length of ICU stay. Hyperlactataemic survivors have a longer LOS and non-survivors a shorter LOS than normal lactate survivors and non-survivors, respectively.
In patients undergoing cardiac surgery, PPVCAP and PPVPC both weakly predict fluid responsiveness. However, COCAP is not a good substitute for COTD and cannot be used to assess fluid responsiveness.
Despite multiple trials of potential therapies for sepsis, no strategies have yet been persistently shown to have beneficial effects on outcomes. The main reason for the disappointing results is that patient populations in these studies have been too heterogeneous. Selecting patients on the basis of general symptoms is not enough. Rather patients should be selected according to the likely action of the drug in question. To achieve this, improved biomarkers of sepsis and of the immune response are needed and the activities of the individual agents need to be carefully characterized. New candidates are being developed and the results of ongoing and recent clinical trials of immunomodulatory therapies are eagerly awaited as new therapies for sepsis are urgently needed.
