Reflex vascular defects in the orthostatic tachycardia syndrome of adolescents

2001 ◽  
Vol 90 (6) ◽  
pp. 2025-2032 ◽  
Author(s):  
Julian M. Stewart ◽  
Amy Weldon
Keyword(s):  
Blood Flow ◽  
Flow Resistance ◽  
Venous Pressure ◽  
Low Flow ◽  
Postural Orthostatic Tachycardia Syndrome ◽  
Venous Compliance ◽  
Calf Blood Flow ◽  
Normal Resistance ◽  
Head Up Tilt ◽  
Normal Controls

Dependent pooling occurs in postural orthostatic tachycardia syndrome (POTS) related to defective vasoconstriction. Increased venous pressure (Pv) >20 mmHg occurs in some patients (high Pv) but not others (normal Pv). We compared 22 patients, aged 12–18 yr, with 13 normal controls. Continuous blood pressure and strain-gauge plethysmography were used to measure supine forearm and calf blood flow, resistance, venous compliance, and microvascular filtration, and blood flow and swelling during 70° head-up tilt. Supine, high Pv had normal resistance in arms (26 ± 2 mmHg · ml−1 · 100 ml · min) and legs (34 ± 3 mmHg · ml−1 · 100 ml · min) but low leg blood flow (1.5 ± 0.4 ml · 100 ml−1 · min−1). Supine leg Pv (30 ± 2 vs. 13 ± 1 mmHg in control) exceeded the threshold for edema (isovolumetric pressure = 19 ± 3 mmHg). Supine, normal Pv had high blood flow in arms (4.1 ± 0.2 vs. 3.5 ± 0.2 ml · 100 ml−1 · min−1 in control) and legs (3.8 ± 0.4 vs. 2.7 ± 0.3 ml · 100 ml−1 · min−1 in control) with low resistance. With tilt, calf blood flow increased steadily in POTS with high Pv and transiently increased in normal Pv. Calf volume increased in all POTS patients. Arm blood flow increased in normal Pv only with forearm maintained at heart level. These data suggest that there are (at least) two subgroups of POTS characterized by high Pv and low flow or normal Pv and high flow. These may correspond to abnormalities in local or baroreceptor-mediated vasoconstriction, respectively.

Vascular perturbations in the chronic orthostatic intolerance of the postural orthostatic tachycardia syndrome

2000 ◽  
Vol 89 (4) ◽  
pp. 1505-1512 ◽  
Author(s):  
Julian M. Stewart ◽  
Amy Weldon
Keyword(s):  
Blood Flow ◽  
Orthostatic Intolerance ◽  
Venous Pressure ◽  
Fluid Collection ◽  
Lower Extremities ◽  
Postural Orthostatic Tachycardia Syndrome ◽  
Size Change ◽  
Venous Compliance ◽  
Edema Formation ◽  
Calf Blood Flow

Chronic orthostatic intolerance is often related to the postural orthostatic tachycardia syndrome (POTS). POTS is characterized by upright tachycardia. Understanding of its pathophysiology remains incomplete, but edema and acrocyanosis of the lower extremities occur frequently. To determine how arterial and venous vascular properties account for these findings, we compared 13 patients aged 13–18 yr with 10 normal controls. Heart rate and blood pressure were continuously recorded, and strain-gauge plethysmography was used to measure forearm and calf blood flow, venous compliance, and microvascular filtration while the subject was supine and to measure calf blood flow and calf size change during head-up tilt. Resting venous pressure was higher in POTS compared with control (16 vs. 10 mmHg), which gave the appearance of decreased compliance in these patients. The threshold for edema formation decreased in POTS patients compared with controls (8.3 vs. 16.3 mmHg). With tilt, early calf blood flow increased in POTS patients (from 3.4 ± 0.9 to 12.6 ± 2.3 ml · 100 ml−1 · min−1) but did not increase in controls. Calf volume increased twice as much in POTS patients compared with controls over a shorter time of orthostasis. The data suggest that resting venous pressure is higher and the threshold for edema is lower in POTS patients compared with controls. Such findings make the POTS patients particularly vulnerable for edema fluid collection. This may signify a redistribution of blood to the lower extremities even while supine, accounting for tachycardia through vagal withdrawal.

Lower vascular tone and larger plasma volume in Parkinson's disease with orthostatic hypotension

2011 ◽  
Vol 111 (2) ◽  
pp. 443-448 ◽  
Author(s):  
J. T. Groothuis ◽  
R. A. J. Esselink ◽  
J. P. H. Seeger ◽  
M. J. H. van Aalst ◽  
M. T. E. Hopman ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Blood Flow ◽  
Orthostatic Hypotension ◽  
Vascular Resistance ◽  
Plasma Volume ◽  
Venous Pressure ◽  
Dilution Method ◽  
Significant Difference ◽  
Head Up Tilt

The pathophysiology of orthostatic hypotension in Parkinson's disease (PD) is incompletely understood. The primary focus has thus far been on failure of the baroreflex, a central mediated vasoconstrictor mechanism. Here, we test the role of two other possible factors: 1) a reduced peripheral vasoconstriction (which may contribute because PD includes a generalized sympathetic denervation); and 2) an inadequate plasma volume (which may explain why plasma volume expansion can manage orthostatic hypotension in PD). We included 11 PD patients with orthostatic hypotension (PD + OH), 14 PD patients without orthostatic hypotension (PD − OH), and 15 age-matched healthy controls. Leg blood flow was examined using duplex ultrasound during 60° head-up tilt. Leg vascular resistance was calculated as the arterial-venous pressure gradient divided by blood flow. In a subset of 9 PD + OH, 9 PD − OH, and 8 controls, plasma volume was determined by indicator dilution method with radiolabeled albumin (125I-HSA). The basal leg vascular resistance was significantly lower in PD + OH (0.7 ± 0.3 mmHg·ml−1·min) compared with PD − OH (1.3 ± 0.6 mmHg·ml−1·min, P < 0.01) and controls (1.3 ± 0.5 mmHg·ml−1·min, P < 0.01). Leg vascular resistance increased significantly during 60° head-up tilt with no significant difference between the groups. Plasma volume was significantly larger in PD + OH (3,869 ± 265 ml) compared with PD − OH (3,123 ± 377 ml, P < 0.01) and controls (3,204 ± 537 ml, P < 0.01). These results indicate that PD + OH have a lower basal leg vascular resistance in combination with a larger plasma volume compared with PD − OH and controls. Despite the increase in leg vascular resistance during 60° head-up tilt, PD + OH are unable to maintain their blood pressure.

Decreased skeletal muscle pump activity in patients with postural tachycardia syndrome and low peripheral blood flow

2004 ◽  
Vol 286 (3) ◽  
pp. H1216-H1222 ◽  
Author(s):  
Julian M. Stewart ◽  
Marvin S. Medow ◽  
Leslie D. Montgomery ◽  
Kenneth McLeod
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Blood Volume ◽  
Orthostatic Intolerance ◽  
Low Flow ◽  
Peripheral Blood Flow ◽  
Muscle Pump ◽  
Postural Tachycardia ◽  
Calf Blood Flow ◽  
Skeletal Muscle Pump

Standing translocates thoracic blood volume into the dependent body. The skeletal muscle pump participates in preventing orthostatic intolerance by enhancing venous return. We investigated the hypothesis that skeletal muscle pump function is impaired in postural tachycardia (POTS) associated with low calf blood flow (low-flow POTS) and depends in general on muscle blood flow. We compared 12 subjects that have low-flow POTS with 10 controls and 7 patients that have POTS and normal calf blood flow using strain-gauge plethysmography to measure peripheral blood flow, venous capacitance, and calf muscle pump function. Blood volume was estimated by dye dilution. We found that calf circumference was reduced in low-flow POTS (32 ± 1 vs. 39 ± 3 and 43 ± 3 cm) and, compared with controls and POTS patients with normal blood flow, is related to the reduced fraction of calf venous capacity emptied during voluntary muscle contraction (ejection fraction, 0.52 ± 0.07 vs. 0.76 ± 0.07 and 0.80 ± 0.06). We found that blood flow was linearly correlated ( rp = 0.69) with calf circumference (used as a surrogate for muscle mass). Blood volume measurements were 2.2 ± 0.3 in low-flow POTS vs. 2.6 ± 0.5 in controls ( P = 0.17) and 2.4 ± 0.7 in normal-flow POTS patients. Decreased calf blood flow may reduce calf size in POTS and thereby impair the upright ejective ability of the skeletal muscle pump and further contribute to overall reduced blood flow and orthostatic intolerance in these patients.

Calf blood flow during prolonged tilt in idiopathic dilated cardiomyopathy and after cardiac transplantation

2000 ◽  
Vol 278 (1) ◽  
pp. H239-H248 ◽  
Author(s):  
Søren Galatius ◽  
Henrik Wroblewski ◽  
Vibeke B. Sørensen ◽  
Peter Bie ◽  
Henrik Arendrup ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Right Atrium ◽  
Orthostatic Intolerance ◽  
Muscle Blood Flow ◽  
Severe Congestive Heart Failure ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Skeletal Muscle Blood Flow ◽  
Calf Blood Flow ◽  
Head Up Tilt

In severe congestive heart failure (CHF), abnormal reflex control of calf blood flow during brief head-up tilt that appears to normalize after transplantation (HTX) may be present during prolonged observation also. Therefore, we studied the effect of prolonged (30 min) 50° head-up tilt on calf skeletal muscle blood flow measured by the local133Xe washout method in CHF and after HTX and in patients with the presence vs. absence of native right atrium (+PNA and −PNA, respectively). During brief head-up tilt, skeletal muscle blood flow increased 13 ± 42% in 9 severe CHF patients in contrast to a −28 ± 22% decrease ( P < 0.01) in 11 control subjects, −24 ± 30% decrease in 15 moderate CHF patients ( P < 0.05), −25 ± 14% decrease in 12 patients with recent HTX ( P < 0.01), and −21 ± 24% decrease in 8 patients with distant HTX ( P = 0.06). However, during sustained tilt, blood flow declined to similar levels of that in the other groups in severe CHF. HTX −PNA vs. +PNA showed blunted skeletal muscle vasomotor control ( P < 0.05) and a higher systolic blood pressure (139 ± 14 vs. 125 ± 15 mmHg, P < 0.05) and heart rate (92 ± 10 vs. 83 ± 8 beats/min, P < 0.05). Thus paradox vasodilatation of calf skeletal muscle in severe CHF is present only during brief but not prolonged tilt. This may be one explanation of the rare presence of orthostatic intolerance in CHF and implies only a minor possible role for the abnormality in edema pathogenesis. Removal of all right atrium in HTX has an important hemodynamic impact that may possibly affect later clinical outcome.

Pathophysiological Changes of Flow Patterns of the Blood in Blood, Vessel Diseases

1979 ◽  
Author(s):  
A.M. Ehrly
Keyword(s):  
Blood Flow ◽  
Venous Pressure ◽  
Cell Aggregation ◽  
Low Flow ◽  
Diabetic Patients ◽  
Flow Properties ◽  
Cell Deformability ◽  
Venous Flow ◽  
Venous Diseases ◽  
Ischemic Diseases

Blood flow properties have been found to he impaired as well in arte-ial occlusive diseases as in venous diseases. Increased blood and -yiacna viscosity values are found in arterial and venous diseases. Hed cell deformability is impaired In diabetic and non-diabetic patients with chronic peripheral ischemic diseases. In addition, the hemodynamic situation (poststenotic low flow in arterial diseases, impaired venous flow and Increased venous pressure in venous diseases) locally increases blood viscosity and red cell aggregation. These factors and local hamoconcentration reduce blood flow velocity and may induce thrombosis.

Regulation of arterial blood pressure in the common green iguana

1975 ◽  
Vol 228 (2) ◽  
pp. 386-391 ◽  
Author(s):  
LA Hohnke
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Venous Pressure ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Head Up Tilt ◽  
Carotid Arterial

Arterial blood pressure (ABP) responses to graded hemorrhage and passive head-up tilt were studied in restrained, anesthetized, and unanesthetized iguanas. The ABP fell slowly in response to hemorrhage up to a critical deficit of 35 plus or minus 19% of the estimated blood volume; the rate of ABP fall then increased nearly 40-fold to continued hemorrhage. Increased heart rate and decreased femoral arterial blood flow accompanied progressive hemorrhage. Propranolol (2-3 mug/kg) did not appreciably alter arterial pressure-hemorrhage curves but hemorrhage-induced increases in heart rate were diminished nearly 50%. Atropine had little effect on either the blood pressure or heart rate changes induced by hemorrhage. During passive tilts of 0-90 degrees carotid arterial pressure fell 33% before returning to control levels (2 min). Heart rate increased and femoral arterial blood flow and central venous pressure fell in response to head-up tilts. It is concluded that hemorrhage and passive head-up tilting can induce reflex cardiovascular changes that assist ABP regulation in iguanas.

Upright posture reduces forearm blood flow early in exercise

1999 ◽  
Vol 276 (5) ◽  
pp. R1434-R1442 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Patrick M. McQuillan ◽  
Lawrence I. Sinoway
Keyword(s):  
Blood Flow ◽  
Brachial Artery ◽  
Forearm Blood Flow ◽  
Venous Pressure ◽  
Upright Posture ◽  
Sympathetic Blockade ◽  
Vascular Conductance ◽  
Flow Response ◽  
Head Up Tilt ◽  
Hyperemic Response

The hypothesis that upright posture could modulate forearm blood flow (FBF) early in exercise was tested in six subjects. Both single (2-s duration) and repeated (1-s work/2-s rest cadence for 12 contractions) handgrip contractions (12 kg) were performed in the supine and 70° head-up tilt (HUT) positions. The arm was maintained at heart level to diminish myogenic effects. Baseline brachial artery diameters were assessed at rest in each position. Brachial artery mean blood velocity (MBV; Doppler) and mean arterial pressure (MAP) (Finapres) were measured continuously to calculate FBF and vascular conductance. MAP was not changed with posture. Antecubital venous pressure (Pv) was reduced in HUT (4.55 ± 1.3 mmHg) compared with supine (11.3 ± 1.9 mmHg) ( P < 0.01). For the repeated contractions, total excess FBF (TEF) was reduced in the HUT position compared with supine ( P < 0.02). With the single contractions, peak FBF, peak vascular conductance, and TEF during 30 s after release of the contraction were reduced in the HUT position compared with supine ( P < 0.01). Sympathetic blockade augmented the FBF response to a single contraction in HUT ( P < 0.05) and tended to increase this response while supine ( P = 0.08). However, sympathetic blockade did not attenuate the effect of HUT on peak FBF and TEF after the single contractions. Raising the arm above heart level while supine, to diminish Pv, resulted in FBF dynamics that were similar to those observed during HUT. Alternatively, lowering the arm while in HUT to restore Pv to supine levels restored the peak FBF and vascular conductance responses, but not TEF response, after a single contraction. It was concluded that upright posture diminishes the hyperemic response early in exercise. The data demonstrate that sympathetic constriction restrains the hyperemic response to a single contraction but does not modulate the postural reduction in postcontraction hyperemia. Therefore, the attenuated blood flow response in the HUT posture was largely related to factors associated with diminished venous pressures and not sympathetic vasoconstriction.

Leg vasoconstriction during head-up tilt in patients with autonomic failure is not abolished

2011 ◽  
Vol 110 (2) ◽  
pp. 416-422 ◽  
Author(s):  
Jan T. Groothuis ◽  
Dick H. J. Thijssen ◽  
Jacques W. M. Lenders ◽  
Jaap Deinum ◽  
Maria T. E. Hopman
Keyword(s):  
Blood Flow ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Vascular Resistance ◽  
Autonomic Failure ◽  
Venous Pressure ◽  
Duplex Ultrasound ◽  
System Control ◽  
Head Up Tilt ◽  
Sympathetic Nervous

Maintaining blood pressure during orthostatic challenges is primarily achieved by baroreceptor-mediated activation of the sympathetic nervous system, which can be divided into preganglionic and postganglionic parts. Despite their preganglionic autonomic failure, spinal cord-injured individuals demonstrate a preserved peripheral vasoconstriction during orthostatic challenges. Whether this also applies to patients with postganglionic autonomic failure is unknown. Therefore, we assessed leg vasoconstriction during 60° head-up tilt in five patients with pure autonomic failure (PAF) and two patients with autonomic failure due to dopamine-β-hydroxylase (DBH) deficiency. Ten healthy subjects served as controls. Leg blood flow was measured using duplex ultrasound in the right superficial femoral artery. Leg vascular resistance was calculated as the arterial-venous pressure gradient divided by blood flow. DBH-deficient patients were tested off and on the norepinephrine pro-drug l-threo-dihydroxyphenylserine (l-DOPS). During 60° head-up tilt, leg vascular resistance increased significantly in PAF patients [0.40 ± 0.38 (+30%) mmHg·ml−1·min−1]. The increase in leg vascular resistance was not significantly different from controls [0.88 ± 1.04 (+72%) mmHg·ml−1·min−1]. In DBH-deficient patients, leg vascular resistance increased by 0.49 ± 0.01 (+153%) and 1.52 ± 1.47 (+234%) mmHg·ml−1·min−1 off and on l-DOPS, respectively. Despite the increase in leg vascular resistance, orthostatic hypotension was present in PAF and DBH-deficient patients. Our results demonstrate that leg vasoconstriction during orthostatic challenges in patients with PAF or DBH deficiency is not abolished. This indicates that the sympathetic nervous system is not the sole or pivotal mechanism inducing leg vasoconstriction during orthostatic challenges. Additional vasoconstrictor mechanisms may compensate for the loss in sympathetic nervous system control.

Vascular adaptation to 4 wk of deconditioning by unilateral lower limb suspension

2005 ◽  
Vol 288 (4) ◽  
pp. H1747-H1755 ◽  
Author(s):  
Michiel W. P. Bleeker ◽  
Patricia C. E. De Groot ◽  
Fleur Poelkens ◽  
Gerard A. Rongen ◽  
Paul Smits ◽  
...  
Keyword(s):  
Blood Flow ◽  
Femoral Artery ◽  
Superficial Femoral Artery ◽  
Lower Limb ◽  
Venous Pressure ◽  
Venous Occlusion ◽  
Calf Blood Flow ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Echo Doppler Ultrasound

Physical inactivity or deconditioning is an independent risk factor for atherosclerosis and cardiovascular disease. In contrast to exercise, the vascular changes that occur as a result of deconditioning have not been characterized. We used 4 wk of unilateral lower limb suspension (ULLS) to study arterial and venous adaptations to deconditioning. In contrast to previous studies, this model is not confounded by denervation or microgravity. Seven healthy subjects participated in the study. Arterial and venous characteristics of the legs were assessed by echo Doppler ultrasound and venous occlusion plethysmography. The diameter of the common and superficial femoral artery decreased by 12% after 4 wk of ULLS. Baseline calf blood flow, as measured by plethysmography, decreased from 2.1 ± 0.2 to 1.6 ± 0.2 ml·min−1·dl tissue−1. Both arterial diameter and calf blood flow returned to baseline values after 4 wk of recovery. There was no indication of a decrease in flow-mediated dilation of the superficial femoral artery after ULLS deconditioning. This means that functional adaptations to inactivity are not simply the inverse of adaptations to exercise. The venous pressure-volume curve is shifted downward after ULLS, without any effect on compliance. In conclusion, deconditioning by 4 wk of ULLS causes significant changes in both the arterial and the venous system.

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