703 VASOPRESSIN USE IN SEPTIC SHOCK


 
 
 Recent clinical data suggest that early vasopressin administration may be better than secondary therapy.In current clinical practice of intensive care, catecholamines represent the first-line hemodynamic treatment for septic shock. Despite the recognized efficacy as a vasopressor, the risk / benefit ratio deriving from the use of noradrenaline, especially at medium-high dosages (higher than 0.25 μg / kg / min) is unbalanced towards side effects including respiratory distress, metabolic stress oxidative and cardiac and renal toxicity. However, its trigger differs from that of catechol-amines on several levels. Vasopressin provokes a reduction in cardiac output and its vasoconstrictor activity is heterogeneous on a topographical level. Its administration provokes vasoconstriction in skin, skeletal muscle, adipose tissue, pancreas and thyroid. This vaso-constriction is less apparent in the mesenteric, coronary and cerebral territories under physiological conditions. Its impact on digestive perfusion is under debate. Two studies conducted in patients with septic shock. demonstrated absence of impact of vasopressin on splanchnic circulation. In contrast, in a recent study conducted in animals in a state of endotoxaemic shock, a reduction in digestive perfusion with vasopressin administration was observed. In this study, the association between concomitant AVP and norepinephrine therapy with mortality was evaluated in a cohort of 10 patients suffering from severe septic shock and hospitalized in the intensive care units. We assumed the NA/ argipressin combination saves the doses of the amine and improves the patient's outcome, reducing morbidity and mortality to 28 days.
 
 
 
 This analysis was designed as observational study. The primary end point of the study was the 28-day mortality rate. The secondary endpoints: the length of stay in intensive care; the number of days without the need for organ support (eg, vasopressors, ventilators, or renal replacement therapy); the time required to achieve haemodynamic stability (i.e. the time to reach a MAP of 65 mm Hg: changes in haemodynamic variables; any need for the use of dobutamine or other inotropic agents. Adverse events have been classified as arrhythmias (i.e., ventricular tachycardia, ventricular fibrillation, or atrial fibrillation), myocardial necrosis, skin necrosis, ischaemia of the limbs or distal extremities, or secondary infections. The data were recorded every 6 hours for 48 hours, every 8 hours on days 3, 4 and 5 and once daily on days 6, 7, 14, 21 and 28: vital signs, non-invasive and invasive hemodynamic variables PICCO MONITORING: Cardiac Index-CI, Indexed Stroke Volume- SVI, MAP, MIXED VENOUS O2 SATURATION, Indexed Systemic Vascular Resistance- SVRI, O2 levels in arterial and mixed venous (or central venous) blood.
 
 
 
 Table 1 summarises the data of the cases enrolled. Table I10 ptsMale73%Age: Average±SD; range67.0±11.43;52-81Mortality in ICU1/10Length of stay in ICU24 (20-28)
 
 
 
 Our results demonstrate how associating a continuous infusion of AVP with NA at a dosage between 0.01 and 0.04 IU / min reduces overall NE levels, improves patient outcome, reducing morbidity and mortality at 28 days. and allows us to optimize the amine descalation and ventilatory weaning times.
