RESUMO
BACKGROUND: Microcirculation and macrohemodynamics are severely compromised during septic shock. However, the relationship between these two compartments needs to be further investigated. We hypothesized that early resuscitation restores left ventricular (LV) performance and microcirculatory function but fails to prevent metabolic disorders. We studied the effects of an early resuscitation protocol (ERP) on LV pressure/volume loops-derived parameters, sublingual microcirculation, and metabolic alterations during endotoxic shock. METHODS: Twenty-five pigs were randomized into three groups: LPS group: Escherichia coli lipopolysaccharide (LPS); ERP group: LPS + ERP based on volume expansion, dobutamine, and noradrenaline infusion; Sham group. LV pressure/volume-derived parameters, systemic hemodynamics, sublingual microcirculation, and metabolic profile were assessed at baseline and after completing the resuscitation protocol. RESULTS: LPS significantly decreased LV end-diastolic volume, myocardial contractility, stroke work, and cardiac index (CI). Early resuscitation preserved preload, and myocardial contractility, increased CI and heart rate (p < .05). LPS severely diminished sublingual microvascular flow index (MFI), perfused vascular density (PVD), and the proportion of perfused vessels (PPV), while increased the heterogeneity flow index (HFI) (p < .05). Despite MFI was relatively preserved, MVD, PVD, and HFI were significantly impaired after resuscitation (p < .05). The macro- and microcirculatory changes were associated with increased lactic acidosis and mixed venous O2 saturation when compared to baseline values (p < .05). The scatter plot between mean arterial pressure (MAP) and MFI showed a biphasic relationship, suggesting that the values were within the limits of microvascular autoregulation when MAP was above 71 ± 6 mm Hg (R (2) = 0.63). CONCLUSIONS: Early hemodynamic resuscitation was effective to restore macrohemodynamia and myocardial contractility. Despite MAP and MFI were relatively preserved, the persistent microvascular dysfunction could explain metabolic disorders. The relationship between micro- and systemic hemodynamia and their impact on cellular function and metabolism needs to be further studied during endotoxic shock.
RESUMO
Introducción: el uso de vasoconstrictores puede afectar la capacidad de predecir la respuesta a volumen de los índices dinámicos. Objetivo: analizar los efectos del tono vasomotor aumentado sobre los índices dinámicos en un modelo de hemorragia. Métodos: se estudiaron 12 conejos durante normovolemia, luego de extracción de 20% de la volemia (HEM), durante la infusión de fenilefrina (FEN) y luego de la reposición con hidroxietilalmidón (HEA). Se midieron la presión (PAo) y flujo de la aorta (FAo) infradiafragmática, las presiones venosa central y ventricular izquierda, permitiendo estimar la variación de la presión arterial de pulso (VPP), del volumen sistólico (VVS) y la presión diastólica final del ventrículo izquierdo (PDFVI). Se monitorizó la pulsioximetría obteniendo la variación de la onda de pulso oximétrica (VOP) y la variación del índice pletismográfico (VIP). El tono vasomotor fue estimado mediante la resistencia vascular total (RVT=PAo/FAo) y la complacencia (C=SV/PAo pulso). Resultados: durante HEM todos los índices dinámicos aumentaron (p<0,05). La FEN determinó un descenso del FAo (p<0,05) y un aumento del tono vasomotor (p<0,05), seudonormalizando los índices dinámicos. El HEA normalizó el FAo y los índices dinámicos. La PDFVI no se modificó. Hubo correlación significativa entre la VVS y la VPP, VOP y la VIP durante N, HEM y HEA (sin fenilefrina), no habiendo correlación durante la infusión de fenilefrina. Conclusiones: la fenilefrina redujo los índices dinámicos enmascarando la pérdida de volumen posiblemente por el aumento del tono vasomotor. Este debería considerarse durante la optimización de la reposición con fluidos.
Introduction: the use of de vasoconstrictors may affect the ability to predict fluid responsiveness of dynamic indicators. Objective: to analyze the effects of an increased vasomotor tone on dynamic indicators in a model of hemorrhage. Methods: twelve rabbits were studied during normovolemia, after withdrawal of 20% of blood volume (HEM), during phenylephrine infusion (PHE) and after replacement with hydroxyethyl starch (HES). Measurements of blood pressure and flow of infradiaphragmatic aorta (AoP - AoF), central venous (CVP) and left ventricular (LVP) were performed, thus allowing to estimate the variation of pulse arterial pressure (PAP), of sistolic volumen (SVV) and end-distolic pressure of the left ventricle (LVEDP). Pulse oximetry was monitored to obtain the pulse oximetry wave variation (POV) and the plethysmographic variability index (PVI). Vasomotor tone was estimated by calculating the total vascular resistance (TVR=AoP/AoF) and compliance (C=SV/AoP pulse). Results: during HEM there was an increase in all dynamic indicators (p<0.05). PHE determined a decrease in the AoF (p<0.05) and an increase in the vasomotor tone (p<0.05), resulting in a pseudonormalization of the dynamic indicators. The HES normalized the AoF and the dynamic indicators. LVEDP was not modified. There was a significant correlation between the SVV and the PAP, POV and the PVI during N, HEM and HES (without phenylephrine); there was no correlation during phenylephrine infusion. Conclusions: phenylephrine reduced the dynamic indicators and concealed the volume deficit probably due to an increase of vasomotor tone. This should be taken into account during optimization of fluid replacement.
Introdução: o uso de vasoconstritores pode afetar a capacidade de predizer a resposta a volume dos índices dinâmicos. Objetivo: analisar os efeitos do tônus vasomotor aumentado sobre os índices dinâmicos em um modelo de hemorragia. Métodos: estudaram-se 12 coelhos durante normovolemia, após a extração de 20% da volemia (HEM), durante a infusão de fenilefrina (FEN) e logo após a reposição com hidroxietilalmidon (HEA). Mediram-se a pressão (PAo) e o fluxo da aorta (FAo) infradiafragmatica, as pressões venosa central e ventricular esquerda (VI), permitindo estimar a variação da pressão arterial do pulso (VPP), do volume sistólico (VVS) e a pressão diastólica final do VI (PDFVI). Monitorizou-se a oximetria de pulso obtendo a variação da onda de pulso oximetrica (VOP) e a variação do índice pletismografico (VIP). O tônus vasomotor foi estimado mediante a resistência vascular total (RTV=PAo/FAo) e a complacência (C=SV/PAo pulso). Resultados: durante HEM todos os índices dinâmicos aumentaram (p<0.05). A FEN determinou um descenso do FAo (p<0.05) e um aumento do tônus vasomotor (p<0.05), pseudonormalizando os índices dinâmicos. O HEA normalizou o FAo e os índices dinâmicos. O HEA normalizou o FAo e os índices dinâmicos. A PDFVI não se modificou. Houve correlação significativa entre VVS e a VPP,VOP e a VIP durante N, HEM e HEA (sem fenilefrina), não havendo correlação durante a infusão de fenilefrina. Conclusões: a fenilefrina diminui os índices dinâmicos mascarando a perda do volume possivelmente pelo aumento do tônus vasomotor. Este deveria considerar- se durante a otimização da reposição com fluidos.
RESUMO
Acute pulmonary hypertension (PH) may arise with or without an increase in vascular smooth muscle (VSM) tone. Our objective was to determine how VSM activation affects both the conduit (CF) and wall buffering (BF) functions of the pulmonary artery (PA) during acute PH states. PA instantaneous flow, pressure, and diameter of six sheep were recorded during normal pressure (CTL) and different states of acute PH: 1) passively induced by PA mechanical occlusion (PPH); 2) actively induced by intravenous administration of phenylephrine (APH); and 3) a combination of both (APPH). To evaluate the direct effect of VSM activation, isobaric (PPH vs. APH) and isometric (CTL vs. APPH) analyses were performed. We calculated the local BF from the elastic (EPD) and viscous (etaPD) indexes as etaPD/EPD and the characteristic impedance (ZC) from pressure and flow to evaluate CF as 1/ZC. We also calculated the absolute and normalized cross-sectional pulsatility (PCS and NPCS, respectively), the dynamic compliance (CDYN), the cross-sectional distensibility (DCS), and the pressure-strain elastic modulus (EP). The isobaric analysis showed increase of CF, BF, and etaPD (P < 0.01) and decrease of EPD (P < 0.05) during APH in respect to PPH (concomitant with isobaric VSM activation-induced vasoconstriction, P < 0.01). The isometric analysis showed increase of E(PD) and etaPD (P < 0.01), nonsignificant difference in BF (even in the presence of a significant mean PA pressure rise, from 14 (SD 6) to 25 (SD 8) mmHg, P < 0.01), and decrease in CF (P < 0.01) during APPH respect to CTL. Mechanical occlusions (PPH and APPH) reduced BF (P < 0.01) and increased EPD (P < 0.05) with regard to their previous steady states (CTL and APH). Nonsignificant differences were found in EPD between PPH and APPH. VSM activation (APH and APPH) increased etaPD (P < 0.01) respect to their previous passive states (CTL and PPH), but no significant differences were found within similar levels of VSM activation. In conclusion, VSM plays a relevant role in main pulmonary artery function during acute pulmonary hypertension, because isobaric vasoconstriction induced by VSM activation improves both BF and CF, mainly due to the increase in etaPD concomitant with the arterial compliance. CDYN and DCS were the more pertinent clinical indexes of arterial elasticity. Additionally, the etaPD-mediated preservation of the BF could be evaluated by the geometric related indexes (PCS and NPCS), which appear to be qualitative markers of arterial wall viscosity status.