Role of passive leg raising to evaluate preload responsiveness in patients with cardiogenic shock after ST elevation myocardial infarction (STEMI) treated with inotropic therapy

Background. Optimal cardiac filling is essential for maintaining an adequate cardiac output and organ perfusion in patients with cardiogenic shock (CS) after ST elevation myocardial infarction (STEMI). “Static” hemodynamic parameters including central venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP) have been used to estimate preload, although their predictive value on fluid responsiveness is not accurate in the presence of huge variations of intrathoracic pressure. Passive leg raising (PLR) represents a “self-volume challenge” that could predict fluid response; the transient hemodynamic effect of PLR on left ventricular stroke volume (SV) detect preload responsiveness in patients with CS after STEMI. Hemodynamic stabilization, preload optimization and correct management of inotropic and fluid therapy is of utmost importance in this patients with a low output syndrome. Aim. The aim of this retrospective study was to determine the agreement between PLR and early hemodynamic status of patients with CS after STEMI. Methods. During observation period (16-months), 79 patients were admitted in our ICU for CS after STEMI; patients who required an intraaortic balloon pump (n=15) and/or mechanical ventilation (n=21) and which were not monitored with PiCCO (n=31) were excluded from the analysis. The final pool included in the study was 12 patients. The hemodynamic management of studied patients was based on guideline treatment, and to maintain individual cardiac index between 1.5 and 2.7 L/min/m2, all patients were treated with an inotropic agent. Heart rate (HR), arterial blood pressure (ABP), CVP, PAOP, lactate plasma levels (LAC), SV, intrathoracic blood volume (ITBV), global end- iastolic volume (GEDV), were recorded in a supine position (baseline position) and after patients were in a supine position with the lower limbs elevated 30° to 45°. Each hemodynamic measurement was recorded within the first 5 min. Patients were considered as fluid preload responsiveness if PLR induced SV increased by ≥10%. To optimize systemic afterload and coronary perfusion, mean arterial blood pressure (MAP) was individually maintained between 60 and 75 mmHg using sodium nitroprusside to decrease vascular resistances, or detect preload responsiveness with PLR. When the MAP was lower 60 mmHg. if the patient was nonresponder was used norepinephrine to increase systemic, as clinically indicated. We measured SV using PiCCO monitor, we calculated changes in SV, induced by PLR. Among 12 patients included in this study, 5 had a SV increase of >10% after PLR. Results. In the responders group (n=5) SV was significantly increased by PLR from 47±14 to 50±14 mL (p<0.001). In these patients infusion within 15 min by 100 mL of 6% hydroxyethyl starch (Voluven) increased SV from 47±14 to 53±15 mL (p<0.001). In the non responders group (n=7) SV has not significantly increased by PLR, from 42±12 to 45±11 mL. In these patients volume expansion increased SV of 45±14 mL. Conclusions. Changes in SV and radial pulse pressure induced by PLR are accurate and interchangeable indices for predicting fluid responsiveness in patients with CS after STEMI.