Review Article Valsalva maneuver in phlebologic practice Stefano Ricci 1 , Leo Moro 1 , Girolamo C Minotti 2 , Raffaele A Incalzi 1 and Marianne De Maeseneer 3 Abstract Forced expiration against an airway obstruction was originally described as a method for inflating the Eustachian tubes and is accredited to Antonio Maria Valsalva (1666–1723). The Valsalva maneuver is commonly applied for different diagnostic purposes. Its use for phlebologic diagnosis is the object this review. Venous reflux is the most frequent pathophysiologic mechanism in chronic venous disease. Reflux is easily visualized by duplex ultrasound when properly elicited, in standing position. A simple way to elicit reflux is the so-called ‘‘compression-release maneuver’’: by emptying the muscle reservoir, it determines a centrifugal gradient, dependent on hydrostatic pressure, creating an aspiration system from the superficial to the deep system. The same results are obtained with dynamics tests activating calf muscles. The Valsalva maneuver elicits reflux by a different mechanism, increasing the downstream pressure and, thus, highlighting any connection between the source of reflux and the refluxing vessel. The Valsalva maneuver is typically used to investigate the saphenofemoral junction. When the maneuver is performed correctly, it is very useful to analyse several conditions and different hemodynamic behaviours of the valvular system at the saphenofemoral junction. Negative Valsalva maneuver always indicates valvular competence at the saphenofemoral junction. Reverse flow lasting during the whole strain (positive Valsalva maneuver) indicates incompetence or absence of proximal valves. Coupling Valsalva maneuver to compression-release maneuver, with the sample volume in different saphenofemoral junction sections, may reveal different hemodynamic situations at the saphenofemoral junction, which can be analysed in detail. Keywords Valsalva maneuver, duplex ultrasound, saphenofemoral junction incompetence, pelvic vein incompetence, venous reflux Introduction Forced expiration against an airway obstruction was originally described as a method for inflating the Eustachian tubes and is accredited to Antonio Maria Valsalva (1666–1723). The Valsalva maneuver (VM) is deeply rooted into the history of medicine. 1–4 It is described as follows: an acute rise in intrathoracic and intra-abdominal pressure, brought about by contraction of the trunk muscles, right down to the pelvic floor, against a ‘‘stop,’’ at the glottis, but also more peripher- ally by the tongue in the nasopharynx, or at the lips and nostrils, or even outside the body, as in the blowing up of a column of mercury in a manometer. 3 The cardiovascular response to VM is largely deter- mined by the neuro-hormonal reaction of heart and vessels to fluctuations in thoracic and abdominal pres- sure. As soon as the subject begins the forced expir- ation, the sudden increase of abdominal and thoracic pressure forces arterial blood out of the thorax. This briefly increases the blood pressure (Phase I). Soon after, the stroke volume decreases rapidly since stress slows the venous return to the heart, and the blood pressure declines progressively (Phase II). Secondary to this fall in cardiac output, the parasym- pathetic signaling from the heart activates the nor- epinephrine release and subsequent systemic vasoconstriction. When the subject relaxes at the end of the maneuver (Phase III), the blood pressure decreases, but now the venous return and, conse- quently, the stroke volume normalize. The pressure increases (Phase IV) and since a vasoconstriction is in place, a hyperpressure flash occurs, resulting in loss of flow rate to the general circulation and decreased 1 Centro di Flebologia, Area di Geriatria, Universita ` Campus Bio Medico, Roma, Italy 2 Fondazione San Raffaele, Cittadella Della Carita `, Taranto, Italy 3 Departement of Dermatology, Erasmus MC, Rotterdam, the Netherlands Corresponding author: Stefano Ricci, Universita ` Campus Bio Medico, Via Alvaro del Portillo, 200, Roma, Italy. Email: varicci@tiscali.it Phlebology 0(0) 1–9 ! The Author(s) 2017 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0268355516678513 journals.sagepub.com/home/phl