Efecto del tono vasomotor sobre los índices dinámicos de precarga.: Impacto en la optimización de la reposición con fluidos

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.

Breve historia del reflejo barorreceptor: de Claude Bernard a Arthur C. Guyton. Ilustrada con algunos experimentos clásicos / A brief history of the baroreceptor reflex: From Claude Bernard to Arthur C. Guyton. Illustrated with some classical experiments

El reflejo barorreceptor es poco conocido por la mayoría de los médicos a pesar de que es fundamental en la estabilización de la presión arterial latido a latido y es crucial para la supervivencia. Su fascinante historia es brevemente revisada en este artículo. En 1852 Claude Bernard descubrió que los nervios simpáticos del cuello inervan los vasos sanguíneos de la piel. En 1932 Edgar Douglas Adrian demostró que los nervios simpáticos que inervan los vasos sanguíneos de la piel descargan en forma espontánea a una frecuencia de cuatro a seis por segundo y de esta forma encontró las bases fisiológicas del tono vasomotor. En el siglo XIX Ludwig Traube y Karl Constantine Ewald Hering descubrieron que la presión arterial fluctúa sincrónicamente con la respiración y Sigmund Mayer observó que también existían oscilaciones más lentas no relacionadas con la respiración. En 1921 Heinrich Ewald Hering mostró la existencia de barorreceptores de alta presión en los senos carotideos y probó que la estimulación de los nervios aferentes que inervan estos receptores induce bradicardia e hipotensión. Estos estudios fueron más tarde avanzados por Corneille Heymans quien ganó el premio Nobel por estos estudios en 1938. En la época de los setentas Cowley y Guyton produjeron denervación sino-aórtica en los perros y de esta manera demostraron la importancia fundamental del reflejo barorreceptor en la estabilización de la presión arterial.

The baroreceptor reflex is poorly known by most physicians even though is fundamental in stabilizing the blood pressure on a beat to beat basis and is crucial for survival. Its fascinating history is briefy reviewed in this article. In 1852 Claude Bernard discovered that the sympathetic nerves of the neck innervate the blood vessels of the skin of the rabbit. Edgar Douglas Adrian in 1932 demonstrated that the sympathetic nerves that innervate the blood vessels discharge spontaneously at a rate of 4-6 per second and thus discovered the physiological basis of the vasomotor tone. In the XIX century Ludwig Traube and Karl Constantine Ewald Hering discovered that blood pressure fluctuates synchronously with respiratory movements and Sigmund Mayer observed that there are also slow non respiratory fluctuations of blood pressure. In 1921 Heinrich Ewald Hering found that high pressure baroreceptors are located in the carotid sinuses and demonstrated that the stimulation of the afferent nerve that innervates it induces bradycardia and hypotension. These studies were further advanced by Corneille Heymans who won the Nobel Prize for these studies in 1938. Later Cowley and Guyton produced sino-aortic denervation in dogs and thereby could demonstrate the fundamental importance of the baroreceptor reflex in the stabilization of blood pressure.

Role of the caudal pressor area in the regulation of sympathetic vasomotor tone

It is well known that the ventrolateral medulla contains neurons involved in the tonic and reflex control of the cardiovascular system. Two regions within the ventrolateral medulla were initially identified: the rostral ventrolateral medulla (RVLM) and the caudal ventrolateral medulla (CVLM). Activation of the RVLM raises arterial blood pressure and sympathetic nerve activity, and activation of the CVLM causes opposite effects. The RVLM premotor neurons project directly to sympathetic preganglionic neurons and are involved in the maintenance of resting sympathetic vasomotor tone. A significant proportion of tonic activity in the RVLM sympathetic premotor neurons is driven by neurons located in a third region of the ventrolateral medulla denominated caudal pressor area (CPA). The CPA is a pressor region located at the extreme caudal part of the ventrolateral medulla that appears to have an important role controlling the activity of RVLM neurons. In this brief review, we will address the importance of the ventrolateral medulla neurons for the generation of resting sympathetic tone related to arterial blood pressure control focusing on two regions, the RVLM and the CPA.

The Vasomotor Tone In Vasospastic Angina

To evaluate the coronary vasomotor tone in vasospasic angina, we compared the diameters of non-spastic segments of vasospastic group with those of control group. The internal diameters of each segment of three major coronary arteries were measured on the basal coronary angiogram, and nitroglycerin administration after provocation with ergonovine or acetylcholine. The vasospastic angina group consisted of 26 patients(20 males, 6 females, mean age of 54 years) and control group consisted of 25 patients (7 males, 18 females, mean age of 55 years). The basal coronary arterial diameters in vasospastic angina group were smaller than those in control group(p<0.05) except the distal segment of right coronary artery. The percent dilation ratio in vasospastic angina group was greater than that in control group(p<0.05). In vasospastic angina group there was no significant difference in the degree of constriction after provocation with ergonovine or acetylcholine between proximal and distal segment. These observations suggest that in vasospastic angina, basal coronary arterial tone is increased in the entire coronary arterial tree and the localized spasm may reflect local hyperrespon siveness.