Effects of Leg Muscle Pumping and Tensing on Orthostatic Arterial Pressure: A Study in Normal Subjects and Patients with Autonomic Failure

1994 ◽  
Vol 87 (5) ◽  
pp. 553-558 ◽  
Author(s):  
A. D. J. Ten Harkel ◽  
J. J. Van Lieshout ◽  
W. Wieling
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Healthy Subjects ◽  
Healthy Adult ◽  
Autonomic Failure ◽  
Contour Method ◽  
Orthostatic Blood Pressure ◽  
Leg Muscle

1. The effects of leg muscle pumping (tiptoeing) and tensing (leg-crossing) on orthostatic blood pressure were investigated in six healthy adult subjects (aged 28–34 years) and in seven patients with severe hypoadrenergic orthostatic hypotension (aged 20–65 years). 2. Finger arterial pressure was monitored. Relative changes in left ventricular stroke volume were computed by a pulse contour method. 3. Tiptoeing increased mean arterial pressure (7 ± 5 mmHg) in the healthy subjects, but not in the patients, whereas cardiac output increased in both groups, although by more in the healthy adults than in the patients (35 ± 10% versus 20 ± 11%, P < 0.05). Systemic vascular resistance decreased substantially in both groups while tiptoeing. Leg-crossing did not affect arterial pressure in the healthy subjects, although stroke volume had increased. In contrast, in the patients an increase in cardiac output (16 ± 12%) and mean blood pressure (13 ± 13 mmHg) was observed. 4. Tiptoeing and leg-crossing have different effects on orthostatic blood pressure in healthy adult subjects and in patients with autonomic failure. In normal humans, tiptoeing increases arterial pressure, whereas leg-crossing has little effect. In the patients, in contrast, tiptoeing has little effect, whereas leg-crossing increases arterial pressure considerably. Patients with autonomic failure should be instructed to apply leg-crossing to combat orthostatic dizziness.

Dynamics of Circulatory Adjustments to Head-Up Tilt and Tilt-Back in Healthy and Sympathetically Denervated Subjects

1998 ◽  
Vol 94 (4) ◽  
pp. 347-352 ◽  
Author(s):  
W. Wieling ◽  
J. J. Van Lieshout ◽  
A. D. J. Ten Harkel
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Healthy Subjects ◽  
Mean Blood Pressure ◽  
Head Up Tilt ◽  
Change In Mean

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.

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 ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Crossover Study ◽  
Healthy Subjects ◽  
Lower Body Negative Pressure ◽  
Vasovagal Syncope ◽  
Orthostatic Tolerance ◽  
Healthy Human

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.

Relative effects of fat-, carbohydrate- and protein-containing liquid diets on cardiac output in healthy adult subjects

1992 ◽  
Vol 83 (4) ◽  
pp. 483-487 ◽  
Author(s):  
Susan K. Hawley ◽  
Kevin S. Channer
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Pulse Rate ◽  
Healthy Adult ◽  
Nutritional Composition ◽  
Significant Rise ◽  
Mean Blood Pressure ◽  
Carbohydrate Diet ◽  
Liquid Meal

1. Nine healthy adult subjects consumed four types of proprietary liquid diet of similar volume and calorific value but of different nutritional composition. The effects on resting cardiac output, mean blood pressure and pulse rate were measured. 2. A significant rise in cardiac output occurred with the balanced, protein and carbohydrate diets but not with the fat diet. The greatest rise was seen with the balanced diet. Water alone had no effect on cardiac output. 3. The average time taken to reach peak cardiac output was shortest with the carbohydrate diet and longest with the fat diet. 4. The increases in cardiac output resulted from a rise in both pulse rate and stroke volume. The carbohydrate diet produced the most sustained rise in pulse rate but the least sustained elevation in stroke volume. 5. No significant changes were seen in mean blood pressure when each liquid meal was compared with water. 6. Our data show that the increase in cardiac output with liquid ingestion is related to the dietary components. These effects are additive.

Finger Arterial versus Intrabrachial Pressure and Continuous Cardiac output during Head-up Tilt Testing in Healthy Subjects

1996 ◽  
Vol 91 (2) ◽  
pp. 193-200 ◽  
Author(s):  
Wilbert T. Jellema ◽  
Ben P. M. Imholz ◽  
Jeroen Van Goudoever ◽  
Karel H. Wesseling ◽  
Johannes J. Van Lieshout
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Healthy Subjects ◽  
Pulse Contour Analysis ◽  
Pulse Contour ◽  
Mean Blood Pressure ◽  
Contour Analysis ◽  
Head Up Tilt ◽  
The Difference

1. The aims of this study were to determine the clinical feasibility of continuous, non-invasive Finapres recordings as a replacement for intrabrachial pressure during a 30 min head-up tilt, and the reliability of continuous cardiac output computation by pulse contour analysis from the finger arterial versus the brachial waveform. 2. In eight healthy subjects a 30 min 70° passive head-up tilt was performed. Finger arterial (FINAP) and intrabrachial (IAP) pressures were measured simultaneously. Beat-to-beat changes in stroke volume were computed using a pulse contour algorithm. 3. Accuracy (the group-averaged FINAP—IAP difference) and precision (the SD of the difference) of Finapres measurements were 4 and 9 mmHg for systolic blood pressure, −5 and 9 mmHg for mean blood pressure and −5 and 9 mmHg for diastolic blood pressure. 4. The time course of the FINAP—IAP differences during head-up tilt showed a linear trend (P < 0.001 for all pressure levels). Averaged for the group, the difference increased 7 mmHg for mean blood pressure. The difference in stroke volume computed from FINAP and IAP was 0.3 ± 5% (mean ± SD), and independent of the duration of the tilt (P > 0.05). This difference did not change at low blood pressure levels (0.5 ± 6%). 5. The qualitative performance of the Finapres allows it to be used in the clinical setting as a monitor of sudden changes in blood pressure induced by a 30 min head-up tilt. Relative changes in stroke volume, as obtained by pulse contour analysis of the finger arterial waveform, closely follow intrabrachial values during long-duration head-up tilt and associated arterial hypotension.

Effects of euglycaemic and hypoglycaemic hyperinsulinaemia on sympathetic and parasympathetic regulation of haemodynamics in healthy subjects

2003 ◽  
Vol 105 (3) ◽  
pp. 315-322 ◽  
Author(s):  
Tomi LAITINEN ◽  
Hanna HUOPIO ◽  
Ilkka VAUHKONEN ◽  
Cyril CAMARO ◽  
Juha HARTIKAINEN ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Healthy Subjects ◽  
Peripheral Resistance ◽  
Fold Increase ◽  
Hyperinsulinaemic Hypoglycaemia ◽  
Plasma Adrenaline ◽  
Parasympathetic Regulation

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.

Hypotensive and Regional Haemodynamic Effects of Exercise, Fasted and after Food, in Human Sympathetic Denervation

1998 ◽  
Vol 94 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Sharmini Puvi-Rajasingham ◽  
Gareth D. P. Smith ◽  
Adeola Akinola ◽  
Christopher J. Mathias
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Superior Mesenteric Artery ◽  
Vascular Resistance ◽  
Mesenteric Artery ◽  
Autonomic Failure ◽  
Sympathetic Denervation ◽  
Stroke Distance

1. In human sympathetic denervation due to primary autonomic failure, food and exercise in combination may produce a cumulative blood pressure lowering effect due to simultaneous splanchnic and skeletal muscle dilatation unopposed by corrective cardiovascular reflexes. We studied 12 patients with autonomic failure during and after 9 min of supine exercise, when fasted and after a liquid meal. Standing blood pressure was also measured before and after exercise. 2. When fasted, blood pressure fell during exercise from 162 ± 7/92 ± 4 to 129 ± 9/70 ± 5 mmHg (mean arterial pressure by 22 ± 5%), P < 0.0005. After the meal, blood pressure fell from 159 ± 8/88 ± 6 to 129 ± 6/70 ± 4 mmHg (mean arterial pressure by 22 ± 3%), P < 0.0001, and further during exercise to 123 ± 6/61 ± 3 mmHg (mean arterial pressure by 9 ± 3%), P < 0.01. The stroke distance—heart rate product, an index of cardiac output, did not change after the meal. During exercise, changes in the stroke distance—heart rate product were greater when fasted. 3. Resting forearm and calf vascular resistance were higher when fasted. Calf vascular resistance fell further after exercise when fasted. Resting superior mesenteric artery vascular resistance was lower when fed; 0.19 ± 0.02 compared with 032 ± 0.06, P < 0.05. After exercise, superior mesenteric artery vascular resistance had risen by 82%, to 0.53 ± 0.12, P < 0.05 (fasted) and by 47%, to 0.29 ± 0.05, P < 0.05 (fed). 4. On standing, absolute levels of blood pressure were higher when fasted [83 ± 7/52 ± 7 compared with 71 ± 2/41 ± 3 (fed), each P < 0.05]. Subjects were more symptomatic on standing post-exercise when fed. 5. In human sympathetic denervation, exercise in the fed state lowered blood pressure further than when fasted and worsened symptoms of postural hypotension.

Long-term hemodynamic actions of atrial natriuretic factor (99-126) in conscious sheep

1988 ◽  
Vol 254 (4) ◽  
pp. H811-H815 ◽  
Author(s):  
D. G. Parkes ◽  
J. P. Coghlan ◽  
J. G. McDougall ◽  
B. A. Scoggins
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Blood Volume ◽  
Total Peripheral Resistance ◽  
Atrial Natriuretic Factor ◽  
Peripheral Resistance ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The hemodynamic and metabolic effects of long-term (5 day) infusion of human atrial natriuretic factor (ANF) were examined in conscious chronically instrumented sheep. Infusion of ANF at 20 micrograms/h, a rate below the threshold for an acute natriuretic effect, decreased blood pressure by 9 +/- 1 mmHg on day 5, associated with a fall in calculated total peripheral resistance. On day 1, ANF reduced cardiac output, stroke volume, and blood volume, effects that were associated with an increase in heart rate and calculated total peripheral resistance and a small decrease in blood pressure. On days 4 and 5 there was a small increase in urine volume and sodium excretion. On day 5 an increase in water intake and body weight was observed. No change was seen in plasma concentrations of renin, arginine vasopressin, glucose, adrenocorticotropic hormone, or protein. This study suggests that the short-term hypotensive effect of ANF results from a reduction in cardiac output associated with a fall in both stroke volume and effective blood volume. However, after 5 days of infusion, ANF lowers blood pressure via a reduction in total peripheral resistance.

Breathing through an inspiratory threshold device improves stroke volume during central hypovolemia in humans

2008 ◽  
Vol 104 (5) ◽  
pp. 1402-1409 ◽  
Author(s):  
Kathy L. Ryan ◽  
William H. Cooke ◽  
Caroline A. Rickards ◽  
Keith G. Lurie ◽  
Victor A. Convertino
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Lower Body Negative Pressure ◽  
Systolic Arterial Pressure ◽  
Intrathoracic Pressure ◽  
Subsequent Increase ◽  
Arterial Blood ◽  
Threshold Device ◽  
Inspiratory Resistance

Inspiratory resistance induced by breathing through an impedance threshold device (ITD) reduces intrathoracic pressure and increases stroke volume (SV) in supine normovolemic humans. We hypothesized that breathing through an ITD would also be associated with a protection of SV and a subsequent increase in the tolerance to progressive central hypovolemia. Eight volunteers (5 men, 3 women) were instrumented to record ECG and beat-by-beat arterial pressure and SV (Finometer). Tolerance to progressive lower body negative pressure (LBNP) was assessed while subjects breathed against either 0 (sham ITD) or −7 cmH2O inspiratory resistance (active ITD); experiments were performed on separate days. Because the active ITD increased LBNP tolerance time from 2,014 ± 106 to 2,259 ± 138 s ( P = 0.006), data were analyzed (time and frequency domains) under both conditions at the time at which cardiovascular collapse occurred during the sham experiment to determine the mechanisms underlying this protective effect. At this time point, arterial blood pressure, SV, and cardiac output were higher ( P ≤ 0.005) when breathing on the active ITD rather than the sham ITD, whereas indirect indicators of autonomic activity (low- and high-frequency oscillations of the R-to-R interval) were not altered. ITD breathing did not alter the transfer function between systolic arterial pressure and R-to-R interval, indicating that integrated baroreflex sensitivity was similar between the two conditions. These data show that breathing against inspiratory resistance increases tolerance to progressive central hypovolemia by better maintaining SV, cardiac output, and arterial blood pressures via primarily mechanical rather than neural mechanisms.

Regional vascular resistance vs. conductance: which index for baroreflex responses?

1991 ◽  
Vol 260 (2) ◽  
pp. H632-H637 ◽  
Author(s):  
D. S. O'Leary
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Pressure Regulation ◽  
Differential Analysis ◽  
Initial Value ◽  
Baseline Effect ◽  
Regional Vascular Resistance ◽  
Vascular Beds ◽  
The Relationship

When large changes in baseline blood flow occur in regional vascular beds (i.e., in skeletal muscle between rest and dynamic exercise or in skin between normothermia and hyperthermia) opposite conclusions are often drawn regarding the magnitude of a given vasomotor response (such as baroreflex vasoconstriction during hypotension) using regional resistance versus conductance. This report analyzes the relationship between changes in regional resistance or conductance and the contribution of the responses in the maintenance of blood pressure. The main supposition is that the appropriate index of baroreflex responses should reflect the importance of the response in the maintenance of blood pressure. Through differential analysis of the relationship between changes in resistance and conductance on arterial pressure, it can be seen that in terms of resistance, the effect of a given change in resistance on arterial pressure is greatly dependent on the baseline level of resistance. For conductance, while a modest baseline effect exists when cardiac output changes markedly, at a constant cardiac output, the same change in regional conductance always causes the same change in arterial pressure regardless of the initial value of conductance. Conclusions drawn are that while neither resistance nor conductance is a perfect index of vasomotor responses, changes in conductance far better reflect the importance of the response in pressure regulation than do changes in regional resistance.

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Sympathetic Blockade ◽  
Selective Blockade ◽  
Arterial Blood

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.

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