Stretch syncope in humans: Evidence for symptomatic neural reflex hypotension triggered by stretching of shoulder and upper back muscles.

Abstract

Background: Stretch-induced syncope (SIS) is a poorly understood condition that we hypothesized may be due to a neural reflex hypotensive response triggered by stretching of shoulder/upper back muscles.

Objective: This study compared the impact of shoulder/upper back stretching on heart rate (HR) and blood pressure (BP) responses in patients with SIS, with the findings in controls evaluated for symptoms unrelated to stretching.

Methods: The study population comprised 33 individuals: 9 otherwise healthy patients with SIS and 24 healthy controls. Beat-to-beat HR and systolic BP (SBP) and mean arterial pressure (MAP) responses were recorded during active standing (AS), Valsalva maneuver, and respiratory sinus arrhythmia. Patients with SIS also underwent carotid sinus massage while seated. In addition, all subjects undertook an active shoulder/upper back extension maneuver for approximately 10-15 seconds while keeping forearms still and breathing normally.

Results: Stretch elicited a drop in BP to nadir values of SBP and MAP (95.9 ± 24.2 and 76.2 ± 17.3 mm Hg in patients with SIS and controls, respectively). However, stretch-induced SBP and MAP decrease was greater in patients with SIS (P=.003 and P=.013). Further, the ratio of the ΔHR increase to ΔBP drop was lower (P=.001) during stretch-induced hypotension than during comparable hypotension induced immediately after AS.

Conclusion: Shoulder/upper back stretching induces a transient hypotensive response in humans, with BP fall greater in patients with SIS than in controls. Further, compensatory HR increment associated with stretch-induced hypotension was less in both patients with SIS and controls than comparable transient BP fall with AS, suggesting chronotropic restraint. Thus, SIS results from exaggerated stretch-induced vasodepression with limited compensatory tachycardia favoring a neural reflex mechanism.