Physical countermaneuvers for orthostatic hypotension are specific actions or exercises (eg, leg crossing, squatting, etc.) that can temporarily increase blood pressure and delay syncope in patients with orthostatic hypotension.
In 1992, van Lieshout and colleagues noted that some patients with autonomic failure empirically learned to avert syncope by physical countermaneuvers such as leg crossing, neck flexing, or squatting (van Lieshout et al 1992). Five of 7 patients with hypoadrenergic orthostatic hypotension developed dizziness within 10 minutes of standing (without leg crossing), which was severe enough in 4 patients that they were unable to remain standing. In all cases physical countermaneuvers allowed patients to remain standing for at least 10 minutes. Leg crossing by putting "one stretched leg in direct contact with the other" for 30 seconds raised the mean blood pressure by 14 mm Hg (SD 6 mm Hg). When blood pressure again became low, patients squatted in 1 to 2 seconds and remained in that position for 30 seconds, raising mean blood pressure by 44 mm Hg (SD 18 mm Hg). Neither maneuver had a large impact on healthy controls. The authors suggested that increased venous return was responsible for the improvement in the patients with orthostatic hypotension. The improvement in venous return was thought to be caused by moving blood from the leg veins and possibly also from the splanchnic vascular bed by abdominal compression.
In 1996, Bouvette and colleagues systematically evaluated 9 subjects with neurogenic orthostatic hypotension (Bouvette et al 1996). They studied 9 different possible maneuvers: squatting, genuflection-contraction (ie, kneeling on 1 knee with flexion and extension at the waist), leg crossing, knee flexion (ie, marching in place), toe raises (ie, repetitively rising onto the balls of the feet and maintaining gastrocnemius contraction for 5 to 10 seconds), neck flexion (ie, touching chin to chest and tightening neck muscles), isometric abdominal contraction, isometric thigh (quadriceps) contraction, and combinations of maneuvers. Valsalva straining was specifically avoided with all of the maneuvers. The most dramatic increase in arterial blood pressure occurred with squatting (41 mm Hg increase in systolic blood pressure with SD 23 mm Hg), but this particular maneuver was felt to be least socially acceptable. Abdominal contraction and neck flexion were the least effective, with abdominal contraction not even producing a significant increase and neck flexion producing only a mean increase of 12 mm Hg in systolic blood pressure. Marching, leg crossing, and toe raises each produced an initial increase of 20 to 25 mm Hg in systolic blood pressure. The response to squatting did not improve with training, while the response to leg crossing improved with training (even without biofeedback), and the response to thigh contraction actually declined without biofeedback.
Blood pressure improvement correlated closely with changes in total peripheral resistance but not heart rate or stroke index (Bouvette et al 1996). The maneuvers that were most effective in increasing the peripheral resistance reduced the abnormally high vascular capacitance (caused by autonomic denervation of the vascular bed) either by closing a portion of the vascular bed (eg, with squatting or genuflection-contraction), active muscle contraction, or both. Changes in stroke index varied considerably across different physical countermaneuvers, but increases were most clearly seen in maneuvers involving contraction of lower extremity muscles. The change in heart rate was generally minimal, consistent with the known impaired baroreflexes in patients with neurogenic orthostatic hypotension.
Bouvette and colleagues also evaluated long-term utility of physical countermaneuvers (Bouvette et al 1996). Three to 4 months after completion of 4 training sessions, all of the patients were still using selected physical countermaneuvers on a daily basis (1 to 11 times/day) to counteract orthostatic intolerance, and all of them reported increased confidence, increased standing time with each episode of presyncopal symptoms (mean 8 minutes, SD 6 minutes), and improved overall function. Seven of the 9 patients were using combinations of maneuvers, and 2 were using single maneuvers, but only 2 patients used the same combination, suggesting a large degree of individual preference or individual variability in response to the maneuvers.
In 1997, Smit and colleagues showed that a portable "fishing chair" (height 38 cm) was useful in increasing blood pressure and cardiac output in patients with orthostatic hypotension. Sitting resulted in an increase in venous return and cardiac filling pressure, and hence stroke volume and cardiac output. The degree of augmentation in systolic blood pressure with sitting on a "fishing chair" was somewhat greater than that accomplished by leg crossing with contraction while standing, and the combination of sitting with leg crossing resulted in a further significant improvement in blood pressure: systolic blood pressure increased by 14 mm Hg with leg crossing while standing, 29 mm Hg with leg crossing and contraction while standing, 37 mm Hg with sitting on a fishing chair, and 61 mm Hg with sitting and crossing. A higher "derby chair" (height 48 cm) was less well tolerated because of persistent presyncopal symptoms, as well as the small seat and greater instability. Similarly a lower footstool (height 20 cm) was also less well tolerated because it was felt to be uncomfortable, and patients had difficulty standing up from the low height or experienced recurrent dizziness when doing so.
In 2007, Thijs and colleagues noted that physical countermaneuvers are often impractical for patients with autonomic failure due to Parkinson disease or multiple system atrophy because of impaired motor skills or balance (Thijs et al 2007), a consideration that applied to many elderly patients with symptomatic orthostatic hypotension from whatever cause. Thijs and colleagues sought to apply respiratory countermaneuvers to impact the "respiratory pump" and augment venous return (and thus blood pressure) by making the intrathoracic pressure more negative during inspiration. Such maneuvers need to avoid hyperventilation, though, because hyperventilation-induced hypocapnea can induce hypotension in patients with autonomic failure. Three specific approaches to increasing negative inspiratory intrathoracic pressure were studied: breathing through pursed lips during inspiration, inspiratory sniffing, and inspiratory obstruction with a mechanical device (ie, narrowing of the inspiratory tube of the 2-way nonrebreathing valve). Inspiratory obstruction with the mechanical device increased mean arterial pressure to a degree comparable with leg muscle tensing, while the effects of inspiratory pursed lip breathing and inspiratory sniffing varied considerably across patients and in general depended on concomitant hyperventilation.