The Basic And Clinical Study Of Vascular Waterfall Hemodynamics In Septic Shock

Objective:1. To investigate the effect of mean arterial pressure (MAP) after finished early goal directed therapy (EGDT) on the prognosis of septic shock patients with abnormal tissue perfusion.2. To determine vascular waterfall phenomenon in septic shock and investigate the effects and clinical significance of volume expansion and different doses of norepinephrine on critical closing pressure(Pcc) and systemic mean filling pressure(Pmsf) ant its hemodynamic significance.Methods:1. One hundred and twenty six septic shock patients admitted to the department of Critical Care Medicine, Peking Union Medical College Hospital from January,2012to December2012were retrospectively studied. The end of EGDT was designated0hr. Norepinephrine was used to titrate the MAP to a higher level for6hours if lactate level was higher. Patients were divided into two groups based on serum lactate level at the end of6hr. Hemodynamic data, serum lactate levels(Lac), central venous oxygen saturation(ScvO2), Acute Physiology and Chronic Health Evaluation Ⅱ score(APACHE Ⅱ) score, mean norepinephrine doses (NE), were obtained at0hr and6hr. The outcome of these patients in28-day after diagnosis was recorded.2.(1)Twenty refractory septic shock patients within six hours after shock admitted in the department of Critical Care Medicine, Peking Union Medical College Hospital fromJuly,2012to August,2013were prospectively observed. sixty-two refractory septic shock patients within six hours after shock admitted in the department of Critical Care Medicine, Peking Union Medical College Hospital from August,2012to February,2013were prospectively studied.(2) A central venous catheter was inserted in the right internal jugular vein for central venous pressure (CVP) monitoring in all of patients. A fluid-filled femoral artery catheter was inserted in the right femoral artery in all of patients for pulse indicator continuous cardiac output (PiCCO) monitoring.(3) No spontaneous breathing efforts were observed during the study. Steady-state mean arterial pressure (Pa), CVP, and cardiac output (CO)were measured over the last3seconds of12-second inspiratory hold maneuvers at plateau pressures of5,15,25, and35cm H2O. The resulting values of CVP were plotted against CO in a venous return curve for the4inspiratory hold procedures and a linear regression line was fitted through these data points. Mean systemic filling pressure (Pmsf) was defined as the zero flow intercept of the venous return curve. Similarly, in a ventricular output curve, Pa was plotted against CO for the same inspiratory hold maneuvers. Critical closing pressure (Pcec) was the extrapolation of Pa to zero flow in the ventricular output curve.(4) Determined the vascular waterfall phenomenon according to the gap of estimated Pcc and Pmsf.(5) Measurements were recorded during baseline conditions and after intravascular administration of500mL crystalloid over15minutes to assess its effects on vascular waterfall after intravascular volume expansion for each patient by hemodynamic variables, percutaneous partial oxygen pressure, blood gas analysis.(6) Arterial pressure was titrated to65�'75�'85�'95mmHg, after30min for hemodynamic stability, to assess their effects on vascular waterfall by hemodynamic variables, percutaneous partial oxygen pressure, blood gas analysis.Results:1.28d mortality was46.03%for this group of patients. There were no significant difference in Lac, APACHE Ⅱ scores and hemodynamic variables at0hr between survival group and non-survival group. Compared to non-survival group, MAP was significantly higher at6hr in survivor group,(86.5±9.8mmHg vs.75.2±10.5mmHg). Norepinephrine dose was significantly higher in survival group than non-survival group at6hr in survivor group,[0.72(0.43,1.6)vs.0.48(0.45,1.4)ug/kg/min]. UO was significantly higher than non-survival group at6hr in survivor group,(1.8±1.1ml/kg/hr vs.1.38±1.2ml/kg/hr). Compared to non-survival group, Lac was significantly lower at6hr in survivor group,(5.3±3.8mmol/L vs.2.1±1.7mmol/L). Other hemodynamic variables at6hr were no sinificantly different between survival group and non-survival group. Multiple variables analysis showed that MAP at6hr was an independent death risk factor. The28d mortality was higher in group of high serum lactate level than that in group of normal serum lactate level,(62.5%vs.29%). MAP in normal serum lactate group was significantly higher than that in high serum lactate group at6hr,(85.6±10.3mmHg vs.77.2±10.7mmHg). UO in normal serum lactate group was significantly higher than that in the high serum lactate group at6hr,(1.8±1.2ug/kg/min vs.1.3±0.9ug/kg/min). Other hemodynamic variables were no significantly different between high serum lactate level group and normal serum lactate level group at0hr and6hr. MAP was negatively related to lactate level at6hr. Patients were divided into three groups based on MAP at6hr. Lac was significantly lower in the group of75-85mmHg group than that in the group of less the75mmHg group. There was no significantly difference between group of75-85mmHg and group of more than85mmHg. There were no significant difference between hemodynamic variables between those three groups at6hr.2.(1)①Mean Pmsf was28.31±6.3mmHg, and mean Pcc was49.59±13.6mmHg,(P<0.0001). A mean pressure difference of21.27±11.1mmHg indicating the presence of a vascular waterfall.②The relation between arterial resistance (Ra) and systemic resistance (Rs) appeared highly significant,(P<0.0001).③The relation between Pcc and SVRI was not highly significant, R=0.27(P=0.032).(2)①Pcc increased from42.9±10.0mmHg to44.8±8.9mmHg after volume expansion,(P=0.188).②Pcc-Pmsf was not significantly changed (21.5±8.6mmHg vs.20.5±7.9mmHg, P=0.899) with intravascular volume administration.③Pmsf-CVP (12.2vs.14.5mmHg) and CO(6.0vs.6.8L.min-1) increased significantly with intravascular volume administration,(P0.0001).④The pressure gradient Pa-Pcc (22.9vs.37.2mmHg) increased and SVRI (1662.6vs.1383.7dyn.sec.cm-5. m-2) decreased significantly after the volume expansion (P<0.0001). However, there was no significant difference in venous resistance (Rv) after intravascular volume administration.⑤Saturation of central venous blood (ScvO2)(75.9vs.81.6%) increased significantly after the volume expansion (P<0.05).(3)①Doses of NE increased step by step during the course of Pa increasing from65mmHg to95mmHg(P<0.0001). There was no change in blood temperature during the whole course of this trial.②When Pa increased from65mmHg to75mmHg:Pmsf and CVP increased significantly, while Pmsf-CVP and CO did not change significantly,(P>0.05). Pec also did not change significantly (42.8vs.44.5mmHg). Pa-Pc increased significantly from22.8mmHg to32.6mmHg,(P<0.0001). Ra and Rs increased, while Rv did not changed. PtO2/PaO2and urinary output (UO) increased significantly,(P<0.05). Serum of lactate level, Pv-aCO2, RI decreased significantly (P<0.05). ScvO2、base excess、PH did not change significantly.②When Pa increased from75mmHg to85mmHg:Pmsf, CVP, Pmsf-CVP, Pcc-Pmsf and CO did not change. Pmsf-CVP and Rv increased compared to values when Pa was65mmHg. Pcc did not change significantly (44.5vs.45.4mmHg). Pa-Pcc increased from22.8to41.9mmHg,(P<0.0001); SVRI, Ra, PtO2/PaO2and UO increased significantly (P<0.05), while Lac decreased significantly. ScvO2, Pv-aCO2, BE, PH did not change.④When Pa increased from85mmHg to95mmHg:Pmsf, CVP, Pmsf-CVP, Rv, CO increased significantly. Pcc increased from45.4±8.8mmHg to59.1±14.8mmHg (P<0.05), while Pa-Pcc did not change significantly (41.9vs.40.6mmHg).Pcc-Pmsf increased significantly from17.0±1.8mmHg to24.5±4.0mmHg. Lac and Pv-aCO2increased significantly. PtO2/PaO2and UO decreased significantly. Conclusions:1.(1)28d mortality was very higher for patients with finished EGDT but abnormal tissue perfusion;(2) Appropriate MAP elevation could decrease the level of serum lactate and the28d mortality;(3) It is not enough to look for optimal perfusion pessure according to the present method. It is imperative to do further research to determine optimal perfusion pessure.2.(1) The pressure gradient of21.27mmHg between Pcc and Pmsf indicating the presence of a vascular waterfall in septic shock;(2) Pcc was not affected by CO elevation by intravascular volume administration;(3) Combination Pcc and SVRI could assess the point of action of vasoactive medication;(4) Pcc increasing abruptly indicated thar tissu perfussion begins to deteriorate during the course of MAP elevation with vasoconstrictice agents;(5) The greatest pressure gradient of Pa-Pcc as the perfusion pressure could optimize tissue perfussion efficiently. The pressure rang was75-85mmHg corrisping to the greatest pressure gradient;(6) Pcc could make optimize tissue perfussion pressure individually and quantizing.