Fisiopatología del síncope neuralmente mediado / Pathophysiology of neurally-mediated syncope

Introducción: El síncope neuralmente mediado (SNM) se define como una pérdida súbita y transitoria del estado de alerta debido a una caída brusca de la presión arterial (PA). Objetivos: Describir los mecanismos putativos fisiopatológicos responsables del SNM, el papel del barorreflejo (BR) y la interacción de sus variables hemodinámicas principales: frecuencia cardiaca (FC) y PA. Desarrollo: Existe una desregulación episódica en el control de las variables hemodinámicas (FC y PA) mediadas por el barorreflejo. Durante la bipedestación activa existe una caída profunda y transitoria de la PA sistólica (PAS) debida a la acción de la gravedad sobre la columna de sangre y probablemente también a una vasodilatación refleja producida por inhibición del reflejo vasosimpático. Las anormalidades del BR en el SNM pueden ser debidas a una mayor intensidad de la caída de la PA al ponerse de pie o a una vasoconstricción retardada o incompleta debido a un reflejo vasosimpático insuficiente o retardado. Conclusiones: Los pacientes con SNM tienen en reposo y antes del síncope un estado de hiperactividad simpática. Durante el ortostatismo activo o la inclinación pasiva hay taquicardia excesiva seguida de bradicardia e hipotensión severa. La recuperación de la caída de la PAS está retardada o incompleta

Introduction: Neurally-mediated syncope (NMS) is defined as a transient loss of consciousness due to an abrupt and intermittent drop in blood pressure (BP). Objectives: This study describes the putative pathophysiological mechanisms giving rise to NMS, the role of baroreflex (BR), and the interaction of its main haemodynamic variables: heart rate (HR) and BP. Development: Episodic dysregulation affects control over the haemodynamic variables (HR and BP) mediated by baroreflex mechanisms. During active standing, individuals experience a profound transient drop in systolic BP due to the effect of gravity on the column of blood and probably also because of reflex vasodilation. Abnormalities in the BR in NMS could be due to a more profound drop in BP upon standing, or to delayed or incomplete vasoconstriction resulting from inhibited or delayed sympathetic activity. Conclusions: Sympathetic hyperactivity is present in patients with NMS at rest and before syncope. During active standing or passive tilting, excessive tachycardia may be followed by bradycardia and profound hypotension. Recovery of systolic BP is delayed or incomplete

Pathophysiology of neurally-mediated syncope. / Fisiopatología del síncope neuralmente mediado.

INTRODUCTION: Neurally-mediated syncope (NMS) is defined as a transient loss of consciousness due to an abrupt and intermittent drop in blood pressure (BP). OBJECTIVES: This study describes the putative pathophysiological mechanisms giving rise to NMS, the role of baroreflex (BR), and the interaction of its main haemodynamic variables: heart rate (HR) and BP. DEVELOPMENT: Episodic dysregulation affects control over the haemodynamic variables (HR and BP) mediated by baroreflex mechanisms. During active standing, individuals experience a profound transient drop in systolic BP due to the effect of gravity on the column of blood and probably also because of reflex vasodilation. Abnormalities in the BR in NMS could be due to a more profound drop in BP upon standing, or to delayed or incomplete vasoconstriction resulting from inhibited or delayed sympathetic activity. CONCLUSIONS: Sympathetic hyperactivity is present in patients with NMS at rest and before syncope. During active standing or passive tilting, excessive tachycardia may be followed by bradycardia and profound hypotension. Recovery of systolic BP is delayed or incomplete.