Efectos del reto de líquidos sobre el acople ventrículo arterial en un biomodelo porcino de choque endotóxico / The effect of fluid challenge on ventriculo-arterial coupling in an endotoxic shock swine bio-model

Introducción: el reto de líquidos es una prueba que consiste en administrarlos y medir la respuesta hemodinámica mediante el cambio del gasto cardíaco (GC), aunque solo medir el GC resulta insuficiente. El acople ventrículo-arterial (AVA) (elastancia arterial efectiva/ elastancia telesistólica: Eae/Ets) aparece como una variable que evalúa el estado cardiocirculatorio en forma integral. Objetivo: evaluar el AVA en un biomodelo de choque endotóxico y durante retos de líquidos. Materiales y métodos: biomodelo de choque endotóxico (9 porcinos). Se midieron variables hemodinámicas cada hora desde un tiempo 0 (T0) hasta T6. Se realizaron 5 retos de líquidos entre T0 y T4. El tiempo de hipotensión se denominó TH0. Se calcularon diferencias de medianas de variables entre T0-T4. Se clasificaron los retos en dos grupos según el delta del AVA (AVA posreto-AVA prerreto), en ΔAVA≤0 o >0, se midieron variables antes y después de cada reto. Se determinó la relación lactato/piruvato (L/P) en T0, T3 y T6, se establecieron correlaciones entre la diferencia LP T6-T0 y de variables hemodinámicas. Resultados: el AVA aumentó (1.58 a 2,02, p=0.042) por incremento en la Eae (1.74 a 2,55; p=0.017). El grupo ΔAVA≤0 elevó el GC (4.32 a 5,46, p=0.032) y el poder cardíaco (PC) (0.61 a 0,77, p=0,028). El Δ L/P se correlacionó con el Δ del índice de choque sistólico y diastólico (r=0.73), pero no con el del AVA. Conclusión: durante el choque endotóxico el AVA aumentó de manera significativa. Durante el reto de líquidos el grupo Δ AVA≤0, elevó el GC y PC. El Δ L/P no se correlacionó con variables del AVA.

Introduction: fluid challenges (FCs) consist of measuring hemodynamic response through changes in cardiac output (CO) after fluid administration, although only measuring CO proves insufficient. Ventriculo-arterial coupling (V-A) (effective arterial elastance / tele-systolic elastance: E(a)/Ets) are variables used for a comprehensive cardiac and circulatory status appraisal. Objective: to evaluate V-A in an endotoxic shock bio-model by FCs. Materials and methods: an endotoxic shock bio-model (9 pigs). Hemodynamic variables were measured every hour from time 0 (T0) to T6. Five FCs were performed between T0 and T4. Hypotension time was referred to as HT. The median differences in variables between T0-T4 were calculated. Challenges were classified into two groups according to V-A delta (post-challenge V-A - pre-challenge V-A). In ΔV-A≤0 o>0, variables were measured before and after each FC. The lactate to pyruvate (L/P) ratio was determined at T0, T3 and T6. Correlations between the LP T6-T0 difference and hemodynamic variables, were established. Results: V-A increased (1.58 to 2,02, p=0.042) as Eae increased (1.74 to 2.55; p=0.017). CO (4.32 to 5.46, p=0.032) and cardiac power (CP) (0.61 to 0.77, p=0,028) increased, in the ΔV-AC≤0 group. The ΔLP correlated with the systolic and diastolic shock index (r=0.73), but not with V-A. Conclusion: V-A increased significantly during endotoxic shock. The ΔAVA≤0 group, showed elevated CO and CP during FC. ΔLP did not correlate with any of the V-A variables.

Changes of operative performance of pulse pressure variation as a predictor of fluid responsiveness in endotoxin shock.

Several limitations regarding pulse pressure variation (PPV) use have been reported. Our aim was to describe changes in the PPV operative performance as a predictor of fluid responsiveness during the development of a swine endotoxin shock model and to assess hemodynamic variables associated with PPV changes. A swine porcine endotoxin shock model was established (Escherichia Coli 055:B5 endotoxin) in 7 pigs, and 3 pigs were included in the control group. The endotoxin was infused until the mean arterial pressure (MAP) dropped below 50 mmHg (TH0); then, the model animal was reanimated with fluids and vasopressors. We performed fluid challenges every hour for 6 h. ROC curve analysis and a linear mixed model were performed. The area under the curve of PPV decreased from 0.95 (0.81-1.00) to 0.60 (0.17-1.00) at TH0. Its cutoff increased from 10.5 to 22.00% at TH0. PPV showed an inverse relationship with stroke volume, mean systemic filling pressure, MAP, and systemic vascular resistance (SVR) (p < 0.001, AIC = 111.85). The PPV operative performance as a predictor of fluid responsiveness decreased with the progression of shock. This could lead to an inverse association between PPV and the following variables: MAP and SVR.