Inotropes and vasopressor use in non-ischemic cardiogenic shock: a single-center retrospective study

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Cardiogenic shock (CS) is a syndrome due to primary cardiac dysfunction leading to multiorgan failure and death in up to 50% of cases. Recently an increased prevalence of non-ischemic CS have been reported. Treatment bundles include inotropes and/or vasopressors; however, indications regarding use of vasoactive drugs in CS are characterized by very low evidence (class IIb - level C)(1,2). Purpose We sought to describe the population of non-ischemic CS in our center, focusing on clinical, hemodynamic and pharmacological data in the first 24 hours (including Maximum Vasoactive Inotropic Score – VISMAX) and to investigate any effect of vasoactive drugs on mortality. Methods We carried out a monocentric retrospective study including adult patients admitted to ICU for non-ischemic CS from January 2011 to December 2020. Results 60 patients were included (40% female; 68.5±12.5 y.o). Median duration of ICU stay was 5 [3-10] days; 27 (45%) patients died in ICU. 41 (68,3%) patients had history of arterial hypertension and 33 (55,9%) had known heart failure (in 20 patients due to ischemic cause); 29 (50,9%) patients were previous treated with beta-blockers. No difference in clinical history data were found between dead and survivors. At index event, mean blood pressure (MBP) was 76±25 mmHg, heart rate (HR) was 103±34 bpm and serum lactate were 4,3 [2,2-13,3] mmol/L among overall population. Patients who died had significantly lower MBP (68,7±29,5 vs 81,6±19,9 mmHg; p <0,05), while no difference in arterial lactate and HR was found between those who died and survivors. Vasoactive drugs were administered in 42 (70%) patients during the first 24 hours. Maximum dosages (mcg/kg/min) of inotropes and vasopressors were: epinephrine 0.10 [0,08-0,17], dobutamine 4.75 [3,5-5,0], norepinephrine 0.3 [0,15-0,48] and dopamine 3,56±1,43. VISMAX In the overall population was 20,0 [8,0-38,0]. Despite not significant, we observed higher VISMAX in the first 24 hours in patients who died (24,5 [9,7-55,9] vs 17 [7,4-26,0] p=0,05); this could be due to difference, although not significant, in norepinephrine dose, as other vasoactive drugs levels were similar (Figure 1). At logistic regression no effect of vasoactive drug and VISMAX on ICU mortality was found (p > 0.05 for all). Conclusions Adrenergic inotropes are reported to be related with increase mortality, although the time duration and dosages used in literature are mostly unknown or very high(3,4). In our cohort of ADHF-CS, those drugs at lower dosages, without differences between died and survivors patients, did not demonstrate any effect on mortality.