Leg crossing improves orthostatic tolerance in healthy subjects: a placebo-controlled crossover study

2006 ◽  
Vol 291 (4) ◽  
pp. H1768-H1772 ◽  
Author(s):  
C. T. Paul Krediet ◽  
Johannes J. van Lieshout ◽  
Lysander W. J. Bogert ◽  
Rogier V. Immink ◽  
Yu-Sok Kim ◽  
...  

Vasovagal syncope is the most common cause of transient loss of consciousness, and recurrent vasovagal fainting has a profound impact on quality of life. Physical countermaneuvers are applied as a means of tertiary prevention but have so far only proven useful at the onset of a faint. This placebo-controlled crossover study tested the hypothesis that leg crossing increases orthostatic tolerance. Nine naïve healthy subjects [6 females, median age 25 yr (range 20–41 yr), mean body mass index 23 (SD 2)] were subjected to passive head-up tilt combined with a graded lower body negative pressure challenge (20, 40, and 60 mmHg) determining orthostatic tolerance thrice, in randomized order: 1) control, 2) with leg crossing, and 3) with oral placebo. Blood pressure (Finometer), heart rate, and changes in thoracic blood volume (impedance), stroke volume, and cardiac output (Modelflow) were followed during orthostatic stress. Primary outcome was time to presyncope (systolic blood pressure ≤85 mmHg, heart rate ≥140 beats/min). With leg crossing, orthostatic tolerance increased from 26 ± 2 to 34 ± 2 min (placebo 23 ± 3 min, P < 0.001). During leg crossing, mean arterial pressure (81 vs. 81 mmHg) and cardiac output (95 vs. 94% supine) remained unchanged; heart rate increase was lower (13 vs. 18 beats/min, P < 0.05); stroke volume was higher (79 vs. 74% supine, P < 0.05); and there was a trend toward lower thoracic impedance. Leg crossing increases orthostatic tolerance in healthy human subjects. As a measure of prevention, it is a worthwhile addition to the management of vasovagal syncope.

2003 ◽  
Vol 105 (3) ◽  
pp. 315-322 ◽  
Author(s):  
Tomi LAITINEN ◽  
Hanna HUOPIO ◽  
Ilkka VAUHKONEN ◽  
Cyril CAMARO ◽  
Juha HARTIKAINEN ◽  
...  

The effects of hypoglycaemia during hyperinsulinaemia, occurring under various pathophysiological conditions, on the cardiovascular regulatory system and vasculature are largely unknown. The aim of the present study was to investigate regulatory and haemodynamic responses to acute hyperinsulinaemia and consequent hypoglycaemia in 18 healthy subjects. Blood sampling and 5 min ECG and blood pressure recordings were performed at baseline and during the euglycaemic and hypoglycaemic phases of a hyperinsulinaemic clamp. Heart rate variability (HRV) and blood pressure variability (BPV) were assessed by using power spectral analysis, and baroreflex sensitivity (BRS) was assessed using the cross-spectral method. Stroke volume was assessed from the non-invasive blood pressure signal by the arterial pulse contour method. Euglycaemic hyperinsulinaemia did not change plasma catecholamine concentrations, HRV, BPV, BRS, heart rate, blood pressure, stroke volume, cardiac output or peripheral resistance. However, hyperinsulinaemic hypoglycaemia resulted in an 11.7-fold increase in the plasma adrenaline concentration (from 0.19±0.03 to 1.68±0.32 nmol/l; P<0.001), and a modest 1.3-fold increase in the plasma noradrenaline concentration (from 1.74±0.22 to 2.02±0.19 nmol/l; P<0.05) compared with baseline. Furthermore, we observed significant decreases in diastolic blood pressure (from 68±3 to 60±3 mmHg; P<0.05) and peripheral resistance (from 24.1±1.2 to 18.5±1.1 mmHg·min-1·l-1; P<0.01). Stroke volume and cardiac output increased markedly from the euglycaemic to the hypoglycaemic period only (P<0.01 for both). Hypoglycaemia did not influence HRV, BPV or BRS. Our findings indicate that hyperinsulinaemic hypoglycaemia is characterized by a significant increase in the plasma adrenaline concentration and by decreases in peripheral resistance and blood pressure. Counter-regulation during hyperinsulinaemic hypoglycaemia involves selective adrenomedullary sympathetic activation, and does not influence cardiac parasympathetic regulation or baroreflex control of heart rate.


1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.


2001 ◽  
Vol 281 (2) ◽  
pp. R468-R475 ◽  
Author(s):  
John S. Floras ◽  
Gary C. Butler ◽  
Shin-Ichi Ando ◽  
Steven C. Brooks ◽  
Michael J. Pollard ◽  
...  

Lower body negative pressure (LBNP; −5 and −15 mmHg) was applied to 14 men (mean age 44 yr) to test the hypothesis that reductions in preload without effect on stroke volume or blood pressure increase selectively muscle sympathetic nerve activity (MSNA), but not the ratio of low- to high-frequency harmonic component of spectral power (PL/PH), a coarse-graining power spectral estimate of sympathetic heart rate (HR) modulation. LBNP at −5 mmHg lowered central venous pressure and had no effect on stroke volume (Doppler) or systolic blood pressure but reduced vagal HR modulation. This latter finding, a manifestation of arterial baroreceptor unloading, refutes the concept that low levels of LBNP interrogate, selectively, cardiopulmonary reflexes. MSNA increased, whereas PL/PH and HR were unchanged. This discordance is consistent with selectivity of efferent sympathetic responses to nonhypotensive LBNP and with unloading of tonically active sympathoexcitatory atrial reflexes in some subjects. Hypotensive LBNP (−15 mmHg) increased MSNA and PL/PH, but there was no correlation between these changes within subjects. Therefore, HR variability has limited utility as an estimate of the magnitude of orthostatic changes in sympathetic discharge to muscle.


1997 ◽  
Vol 22 (4) ◽  
pp. 351-367
Author(s):  
Tania L. Culham ◽  
Gabrielle K. Savard

Several studies indicate that carotid baroreflex responsiveness is a good predictor of orthostatic tolerance. Two groups of healthy women with high (HI) and low (LO) carotid baroreflex responsiveness were studied (a) to determine any differences in the level of orthostatic tolerance of the two groups, and (b) to study the hemodynamic strategies used by HI and LO responders to regulate arterial pressure during the orthostatic challenge of lower body negative pressure (LBNP). Orthostatic tolerance was similar between the two groups, whereas the hemodynamic strategies recruited to maintain blood pressure at −40 mmHg LBNP differed: HI responders exhibited greater LBNP-induced decreases in stroke volume and cardiac output, as well as a greater increase in peripheral resistance compared to LO responders (p < .05). In addition, a significant increase in plasma renin activity during LBNP was found in the HI responders only. No significant between-group differences were found in arterial and cardiopulmonary control of vascular resistance or arterial haroreflex control of heart rate during LBNP. Key words: arterial pressure, carotid baroreceptor, lower body negative pressure, orthostatic tolerance, stroke volume


2021 ◽  
Vol 11 (2) ◽  
pp. 169-172
Author(s):  
Andrew Martusevich ◽  
Ivan Bocharin ◽  
Natalia Ronzhina ◽  
Solomon Apoyan ◽  
Levon Dilenyan ◽  
...  

The aim of this research was to study the peculiarities of heart rate variability (HRV) and microcirculation in students, depending on their sport specialization. Methods and Results: Our study included the results of a survey of 96 students from 18 to 21 years of age who were the members of the national teams of their universities in athletics (n=49) and floorball (n=47). For ECG registration and analysis of hemodynamic findings, including those characterizing the HRV, we used the “Medical Soft” sports testing system (“MS FIT Pro”). For monitoring, we used the standard hemodynamic patterns (blood pressure, HR, stroke volume, cardiac output, and others), statistical and spectral indicators of the HRV, as well as an integral criterion of the state of microcirculation. The studied HRV parameters in most students generally were within the age range. At the same time, track and field athletes have large adaptive resources and, consequently, a more optimal level of myocardial fitness, in comparison with floorball players. Conclusion: The orientation of sports training among students affects heart condition.


1960 ◽  
Vol 15 (6) ◽  
pp. 1065-1068 ◽  
Author(s):  
Edward J. Hershgold ◽  
Sheldon H. Steiner

Dogs were accelerated on the Wright-Patterson AFB human centrifuge in positive and transverse vectors. Cardiac output, blood pressure and heart rate were measured, and stroke volume and peripheral resistance calculated. In positive (headward) acceleration, the cardiac output and stroke volume were reduced; the peripheral resistance was increased. In the transverse vectors, the cardiac output was stable or increased; stroke volume was stable, and peripheral resistance was reduced. The results suggest that the circulatory disturbances associated with positive acceleration may limit tolerance to acceleration and that these may be avoided in transverse acceleration. Note: (With the Technical Assistance of Peter Grenell) Submitted on December 3, 1959


2019 ◽  
Vol 33 (1) ◽  
pp. 39-53 ◽  
Author(s):  
Stefan Duschek ◽  
Alexandra Hoffmann ◽  
Casandra I. Montoro ◽  
Gustavo A. Reyes del Paso

Abstract. Chronic low blood pressure (hypotension) is accompanied by symptoms such as fatigue, reduced drive, faintness, dizziness, cold limbs, and concentration difficulties. The study explored the involvement of aberrances in autonomic cardiovascular control in the origin of this condition. In 40 hypotensive and 40 normotensive subjects, impedance cardiography, electrocardiography, and continuous blood pressure recordings were performed at rest and during stress induced by mental calculation. Parameters of cardiac sympathetic control (i.e., stroke volume, cardiac output, pre-ejection period, total peripheral resistance), parasympathetic control (i.e., heart rate variability), and baroreflex function (i.e., baroreflex sensitivity) were obtained. The hypotensive group exhibited markedly lower stroke volume, heart rate, and cardiac output, as well as higher pre-ejection period and baroreflex sensitivity than the control group. Hypotension was furthermore associated with a smaller blood pressure response during stress. No group differences arose in total peripheral resistance and heart rate variability. While reduced beta-adrenergic myocardial drive seems to constitute the principal feature of the autonomic impairment that characterizes chronic hypotension, baroreflex-related mechanisms may also contribute to this state. Insufficient organ perfusion due to reduced cardiac output and deficient cardiovascular adjustment to situational requirements may be involved in the manifestation of bodily and mental symptoms.


1998 ◽  
Vol 94 (4) ◽  
pp. 347-352 ◽  
Author(s):  
W. Wieling ◽  
J. J. Van Lieshout ◽  
A. D. J. Ten Harkel

1. The initial circulatory adjustments induced by head-up tilt and tilt-back were investigated in six healthy subjects (aged 30–58 years) and six patients with orthostatic hypotension due to pure autonomic failure (aged 33–65 years). 2. Continuous responses of finger arterial pressure and heart rate were recorded by Finapres. A pulse contour algorithm applied to the arterial pressure waveform was used to compute stroke volume responses. 3. In the healthy subjects, head-up tilt induced gradual circulatory adjustments. After 1 min upright stroke volume and cardiac output had decreased by 39 ± 9% and 26 ± 10% respectively. Little change in mean blood pressure at heart level (+1 ± 7 mmHg) indicated that systemic vascular resistance had increased by 39 ± 24%. The gradual responses to head-up tilt contrasted with the pronounced and rapid circulatory responses upon tilt-back. After 2–3 s a rapid increase in stroke volume (from 62 ± 8% to 106 ± 10%) and cardiac output (from 81 ± 11% to 118 ± 20%) was observed with an overshoot of mean arterial pressure above supine control values of 16 ± 3 mmHg at 7 s. In the patients a progressive fall in blood pressure on head-up tilt was observed. After 1 min upright mean blood pressure had decreased by 59 ± 8 mmHg. No change in systemic vascular resistance and a larger decrease in stroke volume (60 ± 7%) and cardiac output (53 ± 8%) were found. On tilt-back a gradual recovery of blood pressure was observed. 4. In healthy humans upon head-up tilt neural compensatory mechanisms are very effective in maintaining arterial pressure at heart level. The gradual circulatory adjustments to head-up tilt in healthy subjects contrast with the pronounced and abrupt circulatory changes on tilt-back. In patients with a lack of neural circulatory reflex adjustments, gradual blood pressure decreases to head-up tilt and gradual increases to tilt-back are observed.


1962 ◽  
Vol 202 (6) ◽  
pp. 1171-1174 ◽  
Author(s):  
Theodore Cooper ◽  
Teresa Pinakatt ◽  
Max Jellinek ◽  
Alfred W. Richardson

Hyperthermia of 40.5 C was induced in anesthetized white rats by microwave exposure (2,450-Mc continuous wave, .08 w/cm2). Thermal response was accompanied by increased cardiac output, stroke volume, cardiac work, and heart rate. Blood pressure and total peripheral resistance decreased. Administration of reserpine as a single dose of 2.5 mg/kg body wt. 1 day before the experiment depleted the myocardial norepinephrine, but did not eliminate the accelerated heart rate and increase of cardiac output during hyperthermia. Hyperthermia after reserpine did not alter significantly the stroke volume and blood pressure, and the peripheral resistance decreased. These data suggest that the circulatory adaptation to microwave hyperthermia is mediated not only through the sympathetic nervous system, but by other mechanisms such as direct cardiac response to the increased tissue temperature.


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