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Leg crossing, muscle tensing, squatting, and the crash position are effective against vasovagal reactions solely through increases in cardiac output

¹Department of Internal Medicine, Academic Medical Center/ University of Amsterdam, Amsterdam, The Netherlands; ²Department of Medicine, University of Wisconsin, Madison, Wisconsin

Submitted 5 November 2004 ; accepted in final form 27 June 2005

	ABSTRACT

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Tensing of lower body muscles without or with leg crossing (LBMT, LCMT), whole body tensing (WBT), squatting, and sitting with the head bent between the knees ("crash position," HBK) are believed to abort vasovagal reactions. The underlying mechanisms are unknown. To study these interventions in patients with a clinical history of vasovagal syncope and a vasovagal reaction during routine tilt table testing, we measured blood pressure (BP) continuously with Finapres and derived heart rate, stroke volume, cardiac output (CO), and total peripheral resistance using Modelflow. In series A (n = 12) we compared LBMT to LCMT. In series B (n = 9), WBT was compared with LCMT. In series C (n = 14) and D (n = 9), we tested squatting and HBK. All maneuvers caused an increase in BP, varying from a systolic rise from 77 ± 8 to 104 ± 18 mmHg (P < 0.05) in series A during LBMT to a rise from 70 ± 10 to 123 ± 9 mmHg (P < 0.05) in series B during LCMT. In each maneuver, the BP increase started within 3–5 s from start of the maneuver. In all maneuvers, there was an increase in CO varying from 54 ± 12% of baseline to 94 ± 21% in WBT to a rise from 65 ± 17% to 110 ± 22% in LCMT in series A. No maneuver caused significant change in total peripheral resistance. We conclude that the mechanism underlying the effects of these maneuvers is exclusively an increase in CO.

Modelflow; muscle pump; stroke volume

The presumed mechanism underlying the beneficial effect of physical countermaneuvers on systemic BP is that skeletal muscle tensing of the lower body reinfuses pooled venous blood back to the chest, thereby increasing cardiac filling pressure, stroke volume (SV), and cardiac output (CO) (22). This mechanism has, however, never been documented during vasovagal reactions. In addition, the possibility that physical countermaneuvers increase peripheral vascular resistance should also be considered (3). Skeletal muscle contractions are accompanied by an increase in central command, which is known to increase the sympathetic outflow (14, 17). Finally, isometric contractions up from 10% of maximal power can compress arteries in skeletal muscle (16, 19), and such mechanical increases in total peripheral resistance (TPR) have also been suggested to play a role in the efficacy of physical countermaneuvers (20, 28).

Hypotheses.   The aims of this study were threefold: 1) to investigate the functional mechanisms underlying the effectiveness of the above mentioned physical countermaneuvers (Table 1), 2) to search for clinically relevant differences in BP changes between lower body muscle tensing with (LCMT, Table 1) and without leg crossing (LBMT), respectively, and whole body tensing (WBT), and 3) to document the efficacy of squatting and that of sitting with the head bent between the knees (HBK) as applied in vasovagal reactions.

	METHODS

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At the Academic Medical Center Syncope Unit, patients with vasovagal syncope are instructed how and when to apply physical countermaneuvers during vasovagal reactions provoked by head-up tilting. Usually a symptomatic vasovagal reaction returns after termination of the maneuver. This gives the opportunity to have patients use more than one maneuver to combat a vasovagal reaction and to compare the effects. Table 1 summarizes the maneuvers.

Inclusion.   From a consecutive series of 66 patients who developed a vasovagal reaction during tilt table testing, 26 patients were selected who successfully had applied either of the next two combinations of maneuvers: LBMT and LCMT (series A, n = 9) or WBT and LCMT (series B, n = 12). Patients who had squatted or applied HBK constituted series C (n = 14) and series D (n = 9), respectively. Consequently, there was some overlap between the series of patients.

Medical history in all patients (conducted by the senior investigator W. Wieling) consisted of at least one episode of loss of consciousness, with prodromal symptoms such as diaphoresis, pallor, or visual disturbances ("seeing black spots") in the presence of any of the following triggers: (prolonged) orthostatic stress, pain, or the experience of an unusually strong emotional circumstance. Exclusion criteria for tilt testing were pregnancy or the presence of structural or (possibly) arrythmogenic heart disease that could lead to syncope.

Tilt protocol and maneuvers.   Investigations took place in the morning, at least 1 h after breakfast, in a room with a temperature of 23°C. Patients were strapped by a single torso belt to a manually controlled tilt table with a foot board. After 5 min of supine rest, patients were 60° tilted head up for 20 min. If no vasovagal reaction developed, 0.4 mg of nitroglycerin was administrated sublingually before an additional 15-min tilt (2). Beat-to-beat systolic and diastolic BPs were measured continuously noninvasively by use of Finapres model 5 (TNO Biomedical Instrumentation, Amsterdam, The Netherlands). The finger cuff was applied to the midphalanx of the left middle finger. To avoid hydrostatic level differences, the hand was held at right atrial level in the midaxillary line. Finapres recordings accurately reflect BP changes during orthostatic stress (7). One of the investigators operated a marker pulse to identify the onset and termination of each maneuver. For offline analysis, all signals were digitally stored in a personal computer at a sampling rate of 100 Hz, as well as real-time printed by a thermo-paper writer (Thermal arraycorder WR 7700, Graphtec, Solingen, Germany) for direct inspection and annotation.

Before the test patients had practiced the maneuvers that they performed during the vasovagal reaction. Patients were instructed to avoid straining during performance of the maneuvers.

All maneuvers started at the moment of a rapid fall in BP in association with symptoms of impending syncope (Fig. 1). Each maneuver was sustained for 40–60 s. Half of patients in series A started with LBMT and applied LCMT at faint recurrence; the other half performed these in reverse order. In series B, maneuver order was split similarly.

View larger version (46K): [in this window] [in a new window]   Fig. 1. Top: excerpts from the original (continuous) blood pressure (BP) tracing in a subject (female, 21) from series A, at indicated intervals during the protocol. Bottom 4 panels show derived heart rate (HR), stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR). SV, CO, and TPR are represented as percentage from baseline [%bl, i.e., mean over the interval 2.5 to 3 min after head-up tilt (HUT)]. LCMT and LBMT, tensing of lower body muscles with and without leg crossing, respectively; HDT, head-down tilt. Vertical gray bars indicate the intervals at which hemodynamic parameters were determined for comparison, as described in METHODS.

During all testing, patients were closely monitored by two experienced investigators. In case of syncope during or after a maneuver, the tilt table was tilted down immediately or if the patient was standing they were laid down on the bed.

SV and TPR computation.   From the continuous BP measurement, the arterial pulse wave was analyzed by a pulse wave analysis method, which computes changes in left ventricular SV from the pulsatile systolic area. We used the improved method of Wesseling, as described in detail previously, using the Modelflow program (model-based measurement method based on a nonlinear, 3-element model of the input impedance of the aorta) (8). This methodology tracks rapid changes in SV accurately (compared with gas rebreathing) during leg crossing with and without muscle tensing (23). During conditions with a low systemic BP, the technique provides accurate values for SV and CO (6, 8).

CO was computed as SV times heart rate (HR), and TPR was calculated as mean BP (MBP) divided by CO. MBP was obtained as the integral of pressure over one beat divided by the corresponding interbeat interval.

Analysis.   As baselines, BP, HR, SV, CO, and TPR were averaged over the intervals 4.5 to 5 min supine rest and 2.5 to 3 min head-up tilt, respectively. The same parameters were then determined 1) right before the start of the maneuver over an interval of 3–5 beats and 2) over an interval after onset of each maneuver of 30 s when a stable BP was reached (Fig. 1). SV, CO, and TPR were expressed in percentage of head-up tilted baseline values (%bl).

For each maneuver we compared all parameters before and during the maneuver, using Student’s paired t-tests. In series A and B, we compared the parameters during each of the two maneuvers in each series, also using paired t-tests. P values <0.05 were considered statistically significant.

	RESULTS

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Patient characteristics and hemodynamic base line values are given in Table 2.

View larger version (39K): [in this window] [in a new window]   Fig. 2. Effects of the various maneuvers on mean blood pressure (MBP), HR, SV, CO, and TPR. SV, CO, and TPR are represented as percentage from baseline (%bl, i.e., mean over the interval 2.5 to 3 min after head-up tilt). Each line represents the indexes at the start of and during the maneuver. The dashed lines with the white plotting-dot represent the group means. The graphs on LCMT combine all subjects in series A and B. *Significant change at P < 0.05; NS, nonsignificant. WBT, whole body tensing; HBK, head bent between knees. See Table 1 for further description of maneuvers.

View larger version (22K): [in this window] [in a new window]   Fig. 3. MBP, HR, SV, CO, and TPR in series A (left) and series B (right). SV, CO, and TPR are represented as percentage from baseline. Each line represents the effects in one individual. Thick dashed lines with open circles represent the group means. *Significant difference at P < 0.05; NS: nonsignificant.

	DISCUSSION

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Effects of physical countermaneuvers on CO and peripheral resistance.   There are remarkable resemblances between the effects of the physical countermaneuvers in the present study on CO and those when inflating an antigravity suit at the onset of an impending vasovagal faint (26). CO rises by a factor of 1.3–1.7 in our maneuvers (Tables 3 and 4) and 1.4 during suit inflation (26). In both experiments, CO increased to 100% of baseline upright values (Tables 3 and 4, Ref. 26). In another study in two healthy individuals, squatting caused a factor 1.6 increase in CO measured by dye dilution (11).

In the classical study by Weissler and coworkers (26), inflation of an antigravity suit during an impending vasovagal faint induced an instantaneous increase in central venous pressure. More recently, it was shown that leg muscle tensing during upright free standing also increased central venous pressure instantaneously (24). These observations document the rapid effect of these interventions on right ventricular filling pressure. However, an effect on systemic BP was observed with a latency of 3 s (9, 26). The explanation for this latency is straightforward and was likely due to the time it took to translocate the venous blood from the right ventricle through the pulmonary circulation to the left ventricle and the systemic circulation (27).

In the above-mentioned antigravity suit experiment, the effects of the intervention were solely explained by an increase in CO (determined by the dye-dilution method) (26). No effects were observed on peripheral vascular resistance, and the vasovagal faints reoccurred after deflation of the antigravity suit. Accordingly, none of the physical countermaneuvers in the present study had any significant effect on TPR, and vasovagal reactions reoccurred after release of muscle tensing. The lack of an effect of physical countermaneuvers on vascular resistance may be surprising, but it is not when the time course of the effects of skeletal muscle tensing on sympathetic outflow and systemic vascular resistance under similar circumstances is considered. During preparation and initiation (first minute) of upright leg-cycling exercise in healthy volunteers, muscle sympathetic nerve activity is decreased, suggesting facilitation of increased muscle blood flow (4). During the first minute of sitting static leg exercise (at 30% of maximal voluntary power), muscle sympathetic nerve traffic was also found to decrease. One of the explanations given by the authors is loading of the cardiopulmonary baroreceptors due to the rapidly increased thoracic blood volume (13). In their study, muscle sympathetic activity only started to increase after 1 min of exercise (13). This increase in sympathetic nerve activity is mediated by the muscle chemoreflex, which is activated after 1–2 min of static muscle exercise (14).

In our study, skeletal muscle tensing was only sustained for 40–60 s. Thus an increase in muscle sympathetic outflow and peripheral resistance is not to be expected. Previous observations that show that lower body muscle tensing during orthostatic stress increases orthostatic tolerance but does not increase peripheral vascular resistance (21) and that isolated hand gripping has only a trivial effect on orthostatic tolerance (9) are in excellent agreement with this explanation of the event.

The observation that isometric handgrip does not increase orthostatic tolerance (9) seems in conflict with the observation by Brignole et al. (3) that forceful isometric arm counterpressure maneuvers during free standing are effective to combat vasovagal reactions. We attribute this difference to leg and abdominal contractions that are inevitable during maximal isometric arm exercise in the upright position to stabilize the body.

So far we have attributed the rise in BP during muscle tensing maneuvers to mechanical effects on CO and not to reflex effects. The HR response, however, documents that reflex effects are involved as well. The instantaneous increase in HR at the onset of muscle tensing (Fig. 1, Ref. 9) is a reflex effect by a combination of central command and the muscle-heart reflex (1, 14). Reflex sympathetic stimulation of cardiac contractility at the onset of exercise may have contributed to the increased CO. In contrast to the muscle tensing maneuvers, the crash position (where no skeletal muscle tensing is involved but only passive abdominal compression) subsequently does not increase HR.

In squatting, where compression of arteries would be expected most prominently, TPR also did not change significantly, indicating that mechanical effects on arterial conductance play a minor role in the efficacy of the maneuvers. This corresponds to an earlier study that was unable to show an effect of squatting on TPR (11).

Limitations.   A potential limitation of our study is that we did not objectify levels of skeletal muscle tension. Although we took care that the different maneuvers were performed with comparable effort in all subjects at all times, the lack of its measurement makes muscle tension an uncontrolled variable in the study. We also did not measure possible changes in intra-abdominal and intrathoracic pressure. Especially in whole body tensing, unintentionally increasing intrathoracic pressure (closing the glottis when commencing whole body tensing) may have impaired venous return, thereby not fully effecting the maneuver's potential.

A potential limitation of generalizability lays in our protocol in which we used nitroglycerine to induce a vasovagal reaction. Although this method is widely used and considered by many as a satisfactory model for vasovagal episodes outside the laboratory (2), there are indications that this provocation leads to predominantly CO (i.e., decreased cardiac filling)-mediated vasovagal reactions (5). Among vasovagal episodes outside the laboratory, the bradycardiac and peripheral vasodilatory effects may be more prevalent. This study may thus overestimate the effects of physical countermaneuvers on CO, compared with vasovagal reactions without nitroglycerine provocation.

Clinical use of physical countermaneuvers.   Although there are differences in the BP effects of the investigated maneuvers, they are small and, because all maneuvers prevented syncope, they do not seem clinically relevant. Thus, when advising patients, the daily applicability of each maneuver should be taken into account, and the advice can be customized to the individual patient's ability to perform the maneuver.

Leg crossing (without muscle tensing) could be used in provocative situations as a preventive measure and either lower or whole body muscle tensing seems a reasonable next step when symptoms develop. If symptoms persist, patients could squat, which may be less embarrassing socially than the formerly advocated laying down. The crash position is especially appropriate when syncope occurs while sitting or for patients who have motor disabilities that would prevent squatting or make them more vulnerable in case of collapse. Recognition of prodromal signs is pivotal in the timely institution of any of the maneuvers, and thus the maneuvers do not apply to the relatively small subset of patients who experience syncope without warning. The range of maneuvers in this study could, however, offer physicians and the mainstay of their patients a means of tailoring therapy to the individual patient's needs. By having a short list of readily accomplishable maneuvers, patients could increase control over their symptoms and potentially improve the quality of their lives.

	GRANTS

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C. T. P. Krediet is recipient of Dr. E. Dekker Stipend 2004 (physician before specialty training, T007) from the Netherlands Heart Foundation. W. Wieling is recipient of Netherlands Heart Foundation Grant no. NHS 99-181. The support from the Netherlands Heart Foundation is gratefully acknowledged.

	FOOTNOTES

 

Address for correspondence: C. T. P. Krediet, Academic Medical Center/Univ. of Amsterdam, Dept. of Internal Medicine, F4-222, Meibergdreef 9, 1105AZ, Amsterdam, The Netherlands (e-mail: c.t.krediet{at}amc.nl)

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

	REFERENCES

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