Clinical Update doi: 10.1111/joim.12249
Physical countermeasures to increase orthostatic tolerance W. Wieling1, N. van Dijk2, R. D. Thijs3,4, F. J. de Lange5, C. T. Paul Krediet1 & J. R. Halliwill6 From the 1Department of Internal Medicine, Academic Medical Centre University of Amsterdam, Amsterdam, the Netherlands; 2Family Medicine, Academic Medical Centre University of Amsterdam, Amsterdam, the Netherlands; 3SEIN – Stichting Epilepsie Instellingen Nederland, Heemstede, the Netherlands; 4Department of Neurology, Leiden University Medical Centre, Leiden, the Netherlands; 5Cardiology, Academic Medical Centre University of Amsterdam, Amsterdam, the Netherlands; and 6Department of Human Physiology, University of Oregon, Eugene, OR, USA
Keywords: blood pressure, cardiac output, muscle pump, orthostatic hypotension, syncope, venous return.
Introduction Standing upright challenges the cardiovascular system as the pull of gravity displaces about 70% of the circulating blood volume to below heart level, much of it to the compliant veins of the dependent limbs and the pelvic organs. In patients with autonomic failure due to neurodegenerative diseases, the normal cardiovascular adjustments to this challenge are impaired, and symptomatic orthostatic hypotension becomes a common risk on standing or even sitting quietly. These patients learn to sway and shift, so that the pumping action of the muscles can be utilized to counter gravitational displacement of blood by squeezing venous blood from the legs upward. Augmentation of venous return in the upright posture can also be achieved by deliberate tensing of lower limb and abdominal muscles [1, 2], as depicted in Fig. 1. These clinical observations were the basis for physical countermeasures, which are taught to patients with autonomic failure to combat symptomatic orthostatic hypotension [3–5]. Physical counterpressure manoeuvres specifically generate a counterpressure to oppose gravitational venous pooling (e.g. a single bout of lower-body muscle contraction to translocate blood centrally and sustained tensing of the same muscles to prevent subsequent peripheral pooling in the legs and abdomen). More recently, it has been shown that physical counterpressure manoeuvres are also effective interventions in otherwise healthy subjects with episodic orthostatic syncope due to neurally mediated (i.e. vasovagal reactions) [6, 7] or postexercise syncope [8]. In this narrative review, we will primarily consider these physical counterpressure manoeuvres. Secondarily, we will describe the broader category of physical countermeasures that include breathing manoeuvres and other physical methods, to
oppose orthostasis. Existing external devices, which operate through some of the same physiological principles as these manoeuvres, will only be discussed for proof of principle. The defining characteristic of the manoeuvres described in this review is the fact that they can be employed by patients when a faint is imminent. This is in contrast to devices such as bandages and abdominal belts, which require ongoing use to be effective. We will discuss both early studies in patient with primary autonomic failure due to neurodegenerative diseases, as well as more recent experience obtained in patients with neurally mediated syncope. The physiology and pathophysiology of orthostatic blood pressure control and perfusion of the brain are key factors in understanding how physical countermeasures work. These topics have been reviewed extensively [2, 9–12] and will only be discussed here briefly. Physical counterpressure manoeuvres Muscle tensing It has been reported that intramuscular pressure is related to orthostatic tolerance [2]. Henderson et al. demonstrated that intramuscular pressure measured in the relaxed biceps muscle was decreased after prolonged bed rest (38%), following surgery (35%), during voluntary hyperventilation (28%) and in the absence of air movement over the skin (31%) [13, 14]. These conditions are strongly associated with decreased orthostatic tolerance and a tendency to faint [2, 15]. In addition, intramuscular calf pressure has been shown to be 15–24 and 6–9 mmHg, respectively, in those without and with a tendency to faint during the head-up tilt test using a tilt table with a saddle and suspended legs (Fig. 1) [16]. Although these interesting results from studies performed in the 1930s and early 1940s have
ª 2014 The Association for the Publication of the Journal of Internal Medicine
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W. Wieling et al.
Clinical Update: Manoeuvres improving orthostatic tolerance
muscle tensing during orthostasis. Although the precise neural pathway has not been established [2], recent work by Bernardi et al. demonstrated that carotid baroreflex modulation influences postural sway [23].
Fig. 1 Effect of whole-body muscle tensing on central blood volume and increased venous pooling in patients with decreased intramuscular pressure. Left, mechanical factors play an important role in promoting venous return in the upright posture. Whole-body muscle tensing increases central blood volume, i.e. the amount of blood available for the heart to pump. Right, intramuscular pressure in normal ‘non-fainters’ during quite standing (left) and in patients with tendency to faint (right). From [2]; reproduced with permission.
never been confirmed, it is highly likely that any increase in muscle tension will function to augment intramuscular pressure. Intramuscular pressure can be thought of as a pressure opposing that within the veins. As such, venous distension is determined by the difference in the opposing pressures on each side of the venous wall (i.e. the venous transmural pressure). Increasing pressure outside the vein will therefore reduce venous distension, displacing blood back towards the heart [2]. During quiet standing, the body behaves more or less as an inverted pendulum that sways about the ankles. The static increase in tone of the antigravity muscles that are involved in maintaining upright posture also function to oppose venous pooling in lower limb veins, thereby protecting central blood volume, i.e. the amount of blood available for the heart to pump [13, 14, 17–19]. It is considered that postural sway during quiet standing is able to compensate for otherwise poor orthostatic tolerance [20, 21]. Along these lines, Amberson [22] suggested the possibility of a connection between arterial baroreceptors and skeletal muscle tone, which could serve to increase 70
ª 2014 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine, 2015, 277; 69–82
The first reports of the application of skeletal muscle tensing to prevent fainting reactions were from psychologists interested in the prevention of fainting reactions due to haemophobia. In the € 1980s Ost and Sterness reported that ‘applied tension’ could be used as a behavioural method for treatment of this phobia [24], but the physiological mechanisms underlying its effect remained poorly understood due to the lack of haemodynamic measurements. However, the development in the early 1990s of the Penaz-Wesseling volume-clamp method, combined with the computation of stroke volume by pulse wave analysis, commercially available as the Finapres device, enabled clinical researchers to combine the experiences of individual patients with continuous noninvasive measurements of beat-by-beat changes in arterial pressure [25, 26]. As a result, the underlying haemodynamics of a wide range of movements that simulated every day activities could be investigated, first in patients with symptomatic orthostatic hypotension due to autonomic failure [1, 3] and in recent years as a countermeasure to avert an impending vasovagal faint. Single case reports were published at first [1, 27–31]. Figure 2 shows an example of such work, in which the combination of leg crossing and leg muscle tensing is effective in counteracting an impending vasovagal syncope [32]. Further evidence came from a study by Krediet et al., which included 20 patients [6]. This work confirmed that the combination of leg crossing and leg muscle tensing depicted in Fig. 2 is highly effective. A rise in blood pressure was observed in all 20 subjects, and the vasovagal reaction was averted in five of these individuals. The remaining 15 subjects were able to postpone the faint by an average of 2.5 min. Patients who could completely abort the faint started the manoeuvre at a significantly higher blood pressure level than those patients who could not (79/51 vs. 61/41 mmHg). In a study focusing on the underlying haemodynamic mechanism, Krediet et al. [33] demonstrated that physical counterpressure manoeuvres such as leg crossing, muscle tensing, squatting and the crash position are effective against vasovagal reactions solely through increases in cardiac output as shown in Fig. 3.
W. Wieling et al.
Clinical Update: Manoeuvres improving orthostatic tolerance
(see Fig. 4) [35]. This reinforces the notion that the physiological effects of muscle tensing are mainly mechanical. However, an instantaneous increase in heart rate (see Figs 2 and 3) was also observed during muscle tensing. This indicates that autonomic effects are present as well. The instantaneous increase in heart rate at the onset of muscle tensing is a reflex effect produced by a combination of the muscle mechanoreflexes and central command with inhibition of cardiac vagal tone [26]. Such chronotropic changes at the onset of exercise are generally associated with concurrent increases in cardiac contractility, which may contribute to the increased cardiac output [33].
Fig. 2 Aborting a vasovagal faint by the combination of leg crossing and muscle tensing. Typical vasovagal syncope in a 24-year-old male subject with recurrent syncope during orthostatic stress testing on a tilt table. After crossing of the legs and tensing of leg and abdominal muscles (+) with the patient remaining in the standing position, blood pressure and heart rate quickly recover. The delay in the increase in blood pressure of about five beats is explained by the transit delay of the venous return through the pulmonary circulation. HR, heart rate; BP, blood pressure; bpm, beats/min. From [32]; reproduced with permission.
During the manoeuvres involving muscle tensing, cardiac output increased by a factor of 1.3–1.7 from the low levels during presyncope and was restored to 95–104% of the stable values recorded in the head-up position in the first few minutes of tilt [33]. Systemic vascular resistance responses varied, but remained largely unchanged. Because lower-body muscle tensing is accompanied by a threefold increase in leg blood flow [34], a counteracting presumably reflex-mediated vasoconstriction must occur in other parts of the circulation, such as the nonworking muscle, kidney and splanchnic vascular beds. The rise in cardiac output during muscle tensing is largely attributed to mechanical and not to autonomic effects. The change in cardiac output as produced by leg crossing with muscle tensing is strikingly similar to that which is produced by inflation of an antigravity suit, which is similarly effective at aborting an impending vasovagal faint
It is worth noting that forceful arm tensing manoeuvres, i.e. hand gripping at maximal voluntary force using a rubber ball and arm tensing by gripping one hand with the other and abducting both the arms at the same time [7, 36, 37], are also effective if they are accompanied by whole-body muscle tensing and thereby by an increase in cardiac output. Isometric arm exercises without tensing of large lower-body muscle groups are far less effective and cannot prevent an impending vasovagal faint [6, 38]. Muscle pumping Activation of the muscle venous pump of the legs during tiptoeing or walking, in the presence of competent venous valves, pumps blood back to the heart and partially restores cardiac filling pressure. The leg muscle pump can be considered as a ‘second heart’ [2] and is capable of translocating blood against a substantial pressure gradient (e.g. >90 mmHg). Manoeuvres that use skeletal muscle pumping are heel raises (i.e. plantar flexion; rising on the toes using calf muscles to raise heels off the floor) and repeated knee flexion (i.e. marching in place) [4, 16, 39]. However, their effects on standing blood pressure in patients with autonomic failure vary. The variable responses may stem from differences in the degree of sympathetic vasomotor failure in these patients [40, 41]. Bending Knowledge that bending forward can mitigate orthostatic hypotension dates back to the 1930s [42] i.e. to the time of the first description ª 2014 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine, 2015, 277; 69–82
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Clinical Update: Manoeuvres improving orthostatic tolerance
Fig. 3 Haemodynamics underlying blood pressure rise induced by muscle tensing. Typical vasovagal syncope in a 21year-old female subject with recurrent vasovagal syncope during tilt-table testing [head-down tilt (HDT), i.e. supine; head-up tilt (HUT), i.e during orthostatic stress]. Leg crossing combined with muscle tensing (first grey bar) and lower-body muscle tensing without leg crossing (second grey bar) are very effective in aborting vasovagal faints. The haemodynamic effect is mediated by an increase in cardiac output (CO), as systemic vascular resistance (SVR) remains largely unchanged. BP, blood pressure; HR, heart rate; SV, stroke volume. SV,CO and SVR are represented as percentage (%) from baseline i.e. mean values over 2.5–3 min after HUT. From [33]; reproduced with permission.
It is a useful manoeuvre for patients with autonomic failure to increase blood pressure in the upright posture, as has been reported by many investigators [1, 41, 43] and is shown in Fig. 5.
ECG 160 mmHg RESP.
BRACHIAL ARTERY CARDIAC OUTPUT
O CVP
5 cmH O 2
Fig. 4 Aborting a vasovagal faint following inflation of antigravity suit to 60 mmHg. Note the progressive fall in intra-arterial pressure (trace labelled ‘Brachial artery’). Blue highlighting indicates the period of inflation. Central venous pressure (CVP) increases immediately after inflation. The increase in blood pressure is delayed by about 3 s due to the transit time from the right to the left ventricle (as in Fig. 3). The increase in blood pressure was solely explained by the increase in cardiac output (increase by a factor of 1.4). ECG, electrocardiogram; Resp., respiration. From [35]; reproduced with permission.
of patients with idiopathic orthostatic hypotension in the English literature by Bradbury and Eggleson. 72
ª 2014 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine, 2015, 277; 69–82
The beneficial effect of bending forward in patients with autonomic failure can be ascribed to pronounced abdominal compression and to lowering the head to heart level. Abdominal compression squeezes blood from the compliant splanchnic venous pool towards the heart, resulting in an increase in cardiac output and thereby in arterial pressure [44, 45]. Additionally, lowering the head to heart level shortens the hydrostatic column between the heart and the brain instantaneously by 25–30 cm corresponding to a hydrostatic pressure increase of 15–20 mmHg in mean blood pressure [11]. In patients prone to vasovagal syncope, bending forward is also reported to be a useful manoeuvre to increase orthostatic tolerance. Treatment of fainting patients traditionally consists of lowering the head between the knees whilst sitting (Fig. 6) [46–49]. Likewise, bending forward with hands on knees appears to be a preferred position for many
W. Wieling et al.
Clinical Update: Manoeuvres improving orthostatic tolerance
Fig. 5 Effects of bending forward on blood pressure. Tracing obtained in a 24-year-old female patient with autonomic failure and debilitating orthostatic hypotension. Orthostatic blood pressure response without (upper panel) and with abdominal compression and bending the head (lower panel). Line marked ‘standing’ indicates the duration of the period of standing. Note in the lower panel the increases both in mean arterial pressure and in pulse pressure during abdominal compression and bending the head. From [1]; reproduced with written informed consent of the patient and permission from the publisher.
athletes during recover from vigorous physical activity. Leg crossing The beneficial effect of leg crossing in patients with autonomic failure (Fig. 7) [1, 43, 50, 51] has been attributed to mechanical compression of the veins in the legs, buttocks and abdomen, which displaces gravitationally pooled blood towards the heart and increases thoracic blood volume [39, 52, 53]. This results in an increase in cardiac filling pressure, stroke volume and cardiac output, effectively correcting the symptom-causing reductions in systemic arterial pressure and cerebral blood flow. When leg crossing is practiced routinely, standing systolic/diastolic blood pressure can be increased by ~20/10 mmHg in patients with autonomic failure [3, 4, 9, 39, 43]. Even such a small rise in upright blood pressure may be clinically important, as it may shift mean arterial pressure from just below to just above the critical level of perfusion of the brain [10]. Larger increases of ~30/
15 mmHg can be seen when leg crossing is combined with the additional tensing of the leg musculature, thighs and buttocks. Leg crossing improves orthostatic tolerance in healthy subjects as well as in patients with vasovagal fainting [27, 54–56]. When standing for prolonged periods, healthy humans who have a tendency to faint often unknowingly utilize this leg crossing countermeasure (i.e. the ‘cocktail party posture’ serves a physiological purpose). Sitting By sitting down, the orthostatic load due to gravitational displacement of blood is decreased, resulting in increases in venous return, stroke volume and cardiac output and thereby blood pressure is increased [57, 58]. Portable chairs have been shown to be quite useful for patients who are severely incapacitated by their orthostatic symptoms [59]. We have shown that the beneficial effect of sitting is greater, i.e. blood pressure increases more, when using lower portable chairs [60]. A chair height of about 40 cm may be optimal for ª 2014 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine, 2015, 277; 69–82
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Clinical Update: Manoeuvres improving orthostatic tolerance
position; these movements were effective at increasing seated blood pressure. This ‘hypotensive akathisia’ appeared to be habitual and could be transiently suppressed, yet felt irresistible to the patients [5]. Squatting
Fig. 6 Manoeuvres to combat vasovagal syncope. A 32year-old female patient underwent cardiovascular reflex assessment for recurrent syncope and presyncope of vasovagal origin. A vasovagal reaction with prodromal pallor and sweating occurred whilst the patient was standing in the cardiovascular laboratory. The patient sat down with her head between her knees (crash position) (upper panel). After standing up, the hypotension returned and the patient squatted (middle panel). After standing up from squatting, when hypotension returned again, she was instructed to cross her legs and tense leg, buttock and abdominal muscles (lower panel), which successfully aborted the presyncope. BP, blood pressure. From [49]; reproduced with permission.
many patients, being effective in raising blood pressure and yet not so low as to cause difficulty in rising, although this may be more of a concern for patients with neurodegenerative diseases with motor disability [9, 59]. Leg crossing can increase seated systolic blood pressure considerably in patients with autonomic failure (Fig. 7) [5, 60, 61], whereas the effects in healthy normotensive subjects (on average
Physical countermeasures to increase orthostatic tolerance W. Wieling1, N. van Dijk2, R. D. Thijs3,4, F. J. de Lange5, C. T. Paul Krediet1 & J. R. Halliwill6 From the 1Department of Internal Medicine, Academic Medical Centre University of Amsterdam, Amsterdam, the Netherlands; 2Family Medicine, Academic Medical Centre University of Amsterdam, Amsterdam, the Netherlands; 3SEIN – Stichting Epilepsie Instellingen Nederland, Heemstede, the Netherlands; 4Department of Neurology, Leiden University Medical Centre, Leiden, the Netherlands; 5Cardiology, Academic Medical Centre University of Amsterdam, Amsterdam, the Netherlands; and 6Department of Human Physiology, University of Oregon, Eugene, OR, USA
Keywords: blood pressure, cardiac output, muscle pump, orthostatic hypotension, syncope, venous return.
Introduction Standing upright challenges the cardiovascular system as the pull of gravity displaces about 70% of the circulating blood volume to below heart level, much of it to the compliant veins of the dependent limbs and the pelvic organs. In patients with autonomic failure due to neurodegenerative diseases, the normal cardiovascular adjustments to this challenge are impaired, and symptomatic orthostatic hypotension becomes a common risk on standing or even sitting quietly. These patients learn to sway and shift, so that the pumping action of the muscles can be utilized to counter gravitational displacement of blood by squeezing venous blood from the legs upward. Augmentation of venous return in the upright posture can also be achieved by deliberate tensing of lower limb and abdominal muscles [1, 2], as depicted in Fig. 1. These clinical observations were the basis for physical countermeasures, which are taught to patients with autonomic failure to combat symptomatic orthostatic hypotension [3–5]. Physical counterpressure manoeuvres specifically generate a counterpressure to oppose gravitational venous pooling (e.g. a single bout of lower-body muscle contraction to translocate blood centrally and sustained tensing of the same muscles to prevent subsequent peripheral pooling in the legs and abdomen). More recently, it has been shown that physical counterpressure manoeuvres are also effective interventions in otherwise healthy subjects with episodic orthostatic syncope due to neurally mediated (i.e. vasovagal reactions) [6, 7] or postexercise syncope [8]. In this narrative review, we will primarily consider these physical counterpressure manoeuvres. Secondarily, we will describe the broader category of physical countermeasures that include breathing manoeuvres and other physical methods, to
oppose orthostasis. Existing external devices, which operate through some of the same physiological principles as these manoeuvres, will only be discussed for proof of principle. The defining characteristic of the manoeuvres described in this review is the fact that they can be employed by patients when a faint is imminent. This is in contrast to devices such as bandages and abdominal belts, which require ongoing use to be effective. We will discuss both early studies in patient with primary autonomic failure due to neurodegenerative diseases, as well as more recent experience obtained in patients with neurally mediated syncope. The physiology and pathophysiology of orthostatic blood pressure control and perfusion of the brain are key factors in understanding how physical countermeasures work. These topics have been reviewed extensively [2, 9–12] and will only be discussed here briefly. Physical counterpressure manoeuvres Muscle tensing It has been reported that intramuscular pressure is related to orthostatic tolerance [2]. Henderson et al. demonstrated that intramuscular pressure measured in the relaxed biceps muscle was decreased after prolonged bed rest (38%), following surgery (35%), during voluntary hyperventilation (28%) and in the absence of air movement over the skin (31%) [13, 14]. These conditions are strongly associated with decreased orthostatic tolerance and a tendency to faint [2, 15]. In addition, intramuscular calf pressure has been shown to be 15–24 and 6–9 mmHg, respectively, in those without and with a tendency to faint during the head-up tilt test using a tilt table with a saddle and suspended legs (Fig. 1) [16]. Although these interesting results from studies performed in the 1930s and early 1940s have
ª 2014 The Association for the Publication of the Journal of Internal Medicine
69
W. Wieling et al.
Clinical Update: Manoeuvres improving orthostatic tolerance
muscle tensing during orthostasis. Although the precise neural pathway has not been established [2], recent work by Bernardi et al. demonstrated that carotid baroreflex modulation influences postural sway [23].
Fig. 1 Effect of whole-body muscle tensing on central blood volume and increased venous pooling in patients with decreased intramuscular pressure. Left, mechanical factors play an important role in promoting venous return in the upright posture. Whole-body muscle tensing increases central blood volume, i.e. the amount of blood available for the heart to pump. Right, intramuscular pressure in normal ‘non-fainters’ during quite standing (left) and in patients with tendency to faint (right). From [2]; reproduced with permission.
never been confirmed, it is highly likely that any increase in muscle tension will function to augment intramuscular pressure. Intramuscular pressure can be thought of as a pressure opposing that within the veins. As such, venous distension is determined by the difference in the opposing pressures on each side of the venous wall (i.e. the venous transmural pressure). Increasing pressure outside the vein will therefore reduce venous distension, displacing blood back towards the heart [2]. During quiet standing, the body behaves more or less as an inverted pendulum that sways about the ankles. The static increase in tone of the antigravity muscles that are involved in maintaining upright posture also function to oppose venous pooling in lower limb veins, thereby protecting central blood volume, i.e. the amount of blood available for the heart to pump [13, 14, 17–19]. It is considered that postural sway during quiet standing is able to compensate for otherwise poor orthostatic tolerance [20, 21]. Along these lines, Amberson [22] suggested the possibility of a connection between arterial baroreceptors and skeletal muscle tone, which could serve to increase 70
ª 2014 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine, 2015, 277; 69–82
The first reports of the application of skeletal muscle tensing to prevent fainting reactions were from psychologists interested in the prevention of fainting reactions due to haemophobia. In the € 1980s Ost and Sterness reported that ‘applied tension’ could be used as a behavioural method for treatment of this phobia [24], but the physiological mechanisms underlying its effect remained poorly understood due to the lack of haemodynamic measurements. However, the development in the early 1990s of the Penaz-Wesseling volume-clamp method, combined with the computation of stroke volume by pulse wave analysis, commercially available as the Finapres device, enabled clinical researchers to combine the experiences of individual patients with continuous noninvasive measurements of beat-by-beat changes in arterial pressure [25, 26]. As a result, the underlying haemodynamics of a wide range of movements that simulated every day activities could be investigated, first in patients with symptomatic orthostatic hypotension due to autonomic failure [1, 3] and in recent years as a countermeasure to avert an impending vasovagal faint. Single case reports were published at first [1, 27–31]. Figure 2 shows an example of such work, in which the combination of leg crossing and leg muscle tensing is effective in counteracting an impending vasovagal syncope [32]. Further evidence came from a study by Krediet et al., which included 20 patients [6]. This work confirmed that the combination of leg crossing and leg muscle tensing depicted in Fig. 2 is highly effective. A rise in blood pressure was observed in all 20 subjects, and the vasovagal reaction was averted in five of these individuals. The remaining 15 subjects were able to postpone the faint by an average of 2.5 min. Patients who could completely abort the faint started the manoeuvre at a significantly higher blood pressure level than those patients who could not (79/51 vs. 61/41 mmHg). In a study focusing on the underlying haemodynamic mechanism, Krediet et al. [33] demonstrated that physical counterpressure manoeuvres such as leg crossing, muscle tensing, squatting and the crash position are effective against vasovagal reactions solely through increases in cardiac output as shown in Fig. 3.
W. Wieling et al.
Clinical Update: Manoeuvres improving orthostatic tolerance
(see Fig. 4) [35]. This reinforces the notion that the physiological effects of muscle tensing are mainly mechanical. However, an instantaneous increase in heart rate (see Figs 2 and 3) was also observed during muscle tensing. This indicates that autonomic effects are present as well. The instantaneous increase in heart rate at the onset of muscle tensing is a reflex effect produced by a combination of the muscle mechanoreflexes and central command with inhibition of cardiac vagal tone [26]. Such chronotropic changes at the onset of exercise are generally associated with concurrent increases in cardiac contractility, which may contribute to the increased cardiac output [33].
Fig. 2 Aborting a vasovagal faint by the combination of leg crossing and muscle tensing. Typical vasovagal syncope in a 24-year-old male subject with recurrent syncope during orthostatic stress testing on a tilt table. After crossing of the legs and tensing of leg and abdominal muscles (+) with the patient remaining in the standing position, blood pressure and heart rate quickly recover. The delay in the increase in blood pressure of about five beats is explained by the transit delay of the venous return through the pulmonary circulation. HR, heart rate; BP, blood pressure; bpm, beats/min. From [32]; reproduced with permission.
During the manoeuvres involving muscle tensing, cardiac output increased by a factor of 1.3–1.7 from the low levels during presyncope and was restored to 95–104% of the stable values recorded in the head-up position in the first few minutes of tilt [33]. Systemic vascular resistance responses varied, but remained largely unchanged. Because lower-body muscle tensing is accompanied by a threefold increase in leg blood flow [34], a counteracting presumably reflex-mediated vasoconstriction must occur in other parts of the circulation, such as the nonworking muscle, kidney and splanchnic vascular beds. The rise in cardiac output during muscle tensing is largely attributed to mechanical and not to autonomic effects. The change in cardiac output as produced by leg crossing with muscle tensing is strikingly similar to that which is produced by inflation of an antigravity suit, which is similarly effective at aborting an impending vasovagal faint
It is worth noting that forceful arm tensing manoeuvres, i.e. hand gripping at maximal voluntary force using a rubber ball and arm tensing by gripping one hand with the other and abducting both the arms at the same time [7, 36, 37], are also effective if they are accompanied by whole-body muscle tensing and thereby by an increase in cardiac output. Isometric arm exercises without tensing of large lower-body muscle groups are far less effective and cannot prevent an impending vasovagal faint [6, 38]. Muscle pumping Activation of the muscle venous pump of the legs during tiptoeing or walking, in the presence of competent venous valves, pumps blood back to the heart and partially restores cardiac filling pressure. The leg muscle pump can be considered as a ‘second heart’ [2] and is capable of translocating blood against a substantial pressure gradient (e.g. >90 mmHg). Manoeuvres that use skeletal muscle pumping are heel raises (i.e. plantar flexion; rising on the toes using calf muscles to raise heels off the floor) and repeated knee flexion (i.e. marching in place) [4, 16, 39]. However, their effects on standing blood pressure in patients with autonomic failure vary. The variable responses may stem from differences in the degree of sympathetic vasomotor failure in these patients [40, 41]. Bending Knowledge that bending forward can mitigate orthostatic hypotension dates back to the 1930s [42] i.e. to the time of the first description ª 2014 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine, 2015, 277; 69–82
71
W. Wieling et al.
Clinical Update: Manoeuvres improving orthostatic tolerance
Fig. 3 Haemodynamics underlying blood pressure rise induced by muscle tensing. Typical vasovagal syncope in a 21year-old female subject with recurrent vasovagal syncope during tilt-table testing [head-down tilt (HDT), i.e. supine; head-up tilt (HUT), i.e during orthostatic stress]. Leg crossing combined with muscle tensing (first grey bar) and lower-body muscle tensing without leg crossing (second grey bar) are very effective in aborting vasovagal faints. The haemodynamic effect is mediated by an increase in cardiac output (CO), as systemic vascular resistance (SVR) remains largely unchanged. BP, blood pressure; HR, heart rate; SV, stroke volume. SV,CO and SVR are represented as percentage (%) from baseline i.e. mean values over 2.5–3 min after HUT. From [33]; reproduced with permission.
It is a useful manoeuvre for patients with autonomic failure to increase blood pressure in the upright posture, as has been reported by many investigators [1, 41, 43] and is shown in Fig. 5.
ECG 160 mmHg RESP.
BRACHIAL ARTERY CARDIAC OUTPUT
O CVP
5 cmH O 2
Fig. 4 Aborting a vasovagal faint following inflation of antigravity suit to 60 mmHg. Note the progressive fall in intra-arterial pressure (trace labelled ‘Brachial artery’). Blue highlighting indicates the period of inflation. Central venous pressure (CVP) increases immediately after inflation. The increase in blood pressure is delayed by about 3 s due to the transit time from the right to the left ventricle (as in Fig. 3). The increase in blood pressure was solely explained by the increase in cardiac output (increase by a factor of 1.4). ECG, electrocardiogram; Resp., respiration. From [35]; reproduced with permission.
of patients with idiopathic orthostatic hypotension in the English literature by Bradbury and Eggleson. 72
ª 2014 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine, 2015, 277; 69–82
The beneficial effect of bending forward in patients with autonomic failure can be ascribed to pronounced abdominal compression and to lowering the head to heart level. Abdominal compression squeezes blood from the compliant splanchnic venous pool towards the heart, resulting in an increase in cardiac output and thereby in arterial pressure [44, 45]. Additionally, lowering the head to heart level shortens the hydrostatic column between the heart and the brain instantaneously by 25–30 cm corresponding to a hydrostatic pressure increase of 15–20 mmHg in mean blood pressure [11]. In patients prone to vasovagal syncope, bending forward is also reported to be a useful manoeuvre to increase orthostatic tolerance. Treatment of fainting patients traditionally consists of lowering the head between the knees whilst sitting (Fig. 6) [46–49]. Likewise, bending forward with hands on knees appears to be a preferred position for many
W. Wieling et al.
Clinical Update: Manoeuvres improving orthostatic tolerance
Fig. 5 Effects of bending forward on blood pressure. Tracing obtained in a 24-year-old female patient with autonomic failure and debilitating orthostatic hypotension. Orthostatic blood pressure response without (upper panel) and with abdominal compression and bending the head (lower panel). Line marked ‘standing’ indicates the duration of the period of standing. Note in the lower panel the increases both in mean arterial pressure and in pulse pressure during abdominal compression and bending the head. From [1]; reproduced with written informed consent of the patient and permission from the publisher.
athletes during recover from vigorous physical activity. Leg crossing The beneficial effect of leg crossing in patients with autonomic failure (Fig. 7) [1, 43, 50, 51] has been attributed to mechanical compression of the veins in the legs, buttocks and abdomen, which displaces gravitationally pooled blood towards the heart and increases thoracic blood volume [39, 52, 53]. This results in an increase in cardiac filling pressure, stroke volume and cardiac output, effectively correcting the symptom-causing reductions in systemic arterial pressure and cerebral blood flow. When leg crossing is practiced routinely, standing systolic/diastolic blood pressure can be increased by ~20/10 mmHg in patients with autonomic failure [3, 4, 9, 39, 43]. Even such a small rise in upright blood pressure may be clinically important, as it may shift mean arterial pressure from just below to just above the critical level of perfusion of the brain [10]. Larger increases of ~30/
15 mmHg can be seen when leg crossing is combined with the additional tensing of the leg musculature, thighs and buttocks. Leg crossing improves orthostatic tolerance in healthy subjects as well as in patients with vasovagal fainting [27, 54–56]. When standing for prolonged periods, healthy humans who have a tendency to faint often unknowingly utilize this leg crossing countermeasure (i.e. the ‘cocktail party posture’ serves a physiological purpose). Sitting By sitting down, the orthostatic load due to gravitational displacement of blood is decreased, resulting in increases in venous return, stroke volume and cardiac output and thereby blood pressure is increased [57, 58]. Portable chairs have been shown to be quite useful for patients who are severely incapacitated by their orthostatic symptoms [59]. We have shown that the beneficial effect of sitting is greater, i.e. blood pressure increases more, when using lower portable chairs [60]. A chair height of about 40 cm may be optimal for ª 2014 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine, 2015, 277; 69–82
73
W. Wieling et al.
Clinical Update: Manoeuvres improving orthostatic tolerance
position; these movements were effective at increasing seated blood pressure. This ‘hypotensive akathisia’ appeared to be habitual and could be transiently suppressed, yet felt irresistible to the patients [5]. Squatting
Fig. 6 Manoeuvres to combat vasovagal syncope. A 32year-old female patient underwent cardiovascular reflex assessment for recurrent syncope and presyncope of vasovagal origin. A vasovagal reaction with prodromal pallor and sweating occurred whilst the patient was standing in the cardiovascular laboratory. The patient sat down with her head between her knees (crash position) (upper panel). After standing up, the hypotension returned and the patient squatted (middle panel). After standing up from squatting, when hypotension returned again, she was instructed to cross her legs and tense leg, buttock and abdominal muscles (lower panel), which successfully aborted the presyncope. BP, blood pressure. From [49]; reproduced with permission.
many patients, being effective in raising blood pressure and yet not so low as to cause difficulty in rising, although this may be more of a concern for patients with neurodegenerative diseases with motor disability [9, 59]. Leg crossing can increase seated systolic blood pressure considerably in patients with autonomic failure (Fig. 7) [5, 60, 61], whereas the effects in healthy normotensive subjects (on average
