Contrasting neurovascular findings in chronic orthostatic intolerance and neurocardiogenic syncope

2003 ◽  
Vol 104 (4) ◽  
pp. 329-340 ◽  
Author(s):  
Julian M. STEWART ◽  
Amy WELDON

Simple faint (neurocardiogenic syncope) and postural tachycardia syndrome (POTS) characterize acute and chronic orthostatic intolerance respectively. We explored the hypothesis that vascular function is similar in the two conditions. We studied 29 patients with POTS and compared them with 20 patients with neurocardiogenic syncope who were otherwise well, and with 15 healthy control subjects. We measured continuous heart rate, respiration and blood pressure, and used venous occlusion strain gauge plethysmography to measure calf and forearm blood flow, peripheral arterial resistance, peripheral venous resistance and venous pressure (Pv). Upright tilt was performed to 70° for 10min, during which calf blood flow and volume were measured. Calf Pv was increased (to 27.2±2.0mmHg) in a subgroup of POTS patients, who also had increased arterial resistance (57±6mmHg·ml-1·min-1·100ml-1 tissue), increased venous resistance (2.4±0.3mmHg·ml-1·min-1·100ml-1 tissue), and decreased peripheral flow (1.0±0.2ml·min-1·100ml-1 tissue) in the calf; other POTS patients with a normal Pv had decreased arterial resistance (18±2mmHg·ml-1·min-1·100ml-1 tissue) and increased blood flow (3.8±0.3ml·min-1·100ml-1 tissue). Syncope patients were not different from controls (Pv = 11.4±0.5mmHg; calf flow = 3.1±0.2ml·min-1·100ml-1 tissue; arterial resistance = 27±2mmHg·ml-1·min-1·100ml-1 tissue; venous resistance = 1.2±0.3mmHg·ml-1·min-1·100ml-1 tissue). When upright, syncope patients and control subjects had similar increases in heart rate and calf volume, stable blood pressure, and decreases in blood flow. POTS patients had markedly increased heart rate and calf blood flow, unstable blood pressure, and pooling in the lower extremities, regardless of subgroup. We conclude that peripheral vascular physiology in patients with POTS is abnormal, in contrast with normal peripheral vascular physiology in neurocardiogenic syncope.

2016 ◽  
Vol 2016 ◽  
pp. 1-20 ◽  
Author(s):  
Peter Novak

Objective. The head-up tilt test is widely used for evaluation of orthostatic intolerance. Although orthostatic symptoms usually reflect cerebral hypoperfusion, the cerebral blood flow velocity (CBFv) profile in orthostatic syndromes is not well described. This study evaluated CBFv and cardiovascular patterns associated with the tilt test in common orthostatic syndromes. Methods. This retrospective study analyzed the tilt test of patients with history of orthostatic intolerance. The following signals were recorded: ECG, blood pressure, CBFv using transcranial Doppler, respiratory signals, and end tidal CO2. Results. Data from 744 patients were analyzed. Characteristic pattern associated with a particular orthostatic syndrome can be grouped into abnormalities predominantly affecting blood pressure (orthostatic hypotension, orthostatic hypertension syndrome, vasomotor oscillations, and neurally mediated syncope—cardioinhibitory, vasodepressor, and mixed), cerebral blood flow (orthostatic hypoperfusion syndrome, primary cerebral autoregulatory failure), and heart rate (tachycardia syndromes: postural tachycardia syndrome, paroxysmal sinus tachycardia, and inappropriate sinus tachycardia). Psychogenic pseudosyncope is associated with stable CBFv. Conclusions. The tilt test is useful add-on in diagnosis of several orthostatic syndromes. However diagnostic criteria for several syndromes had to be modified to allow unambiguous pattern classification. CBFv monitoring in addition to blood pressure and heart rate may increase diagnostic yield of the tilt test.


2005 ◽  
Vol 289 (5) ◽  
pp. H1951-H1959 ◽  
Author(s):  
Julian M. Stewart ◽  
Marvin S. Medow ◽  
Leslie D. Montgomery ◽  
June L. Glover ◽  
Mark M. Millonas

Prior work demonstrated dependence of the change in blood pressure during the Valsalva maneuver (VM) on the extent of thoracic hypovolemia and splanchnic hypervolemia. Thoracic hypovolemia and splanchnic hypervolemia characterize certain patients with postural tachycardia syndrome (POTS) during orthostatic stress. These patients also experience abnormal phase II hypotension and phase IV hypertension during VM. We hypothesize that reduced splanchnic arterial resistance explains aberrant VM results in these patients. We studied 17 POTS patients aged 15–23 yr with normal resting peripheral blood flow by strain gauge plethysmography and 10 comparably aged healthy volunteers. All had normal blood volumes by dye dilution. We assessed changes in estimated thoracic, splanchnic, pelvic-thigh, and lower leg blood volume and blood flow by impedance plethysmography throughout VM performed in the supine position. Baseline splanchnic blood flow was increased and calculated arterial resistance was decreased in POTS compared with control subjects. Splanchnic resistance decreased and flow increased in POTS subjects, whereas splanchnic resistance increased and flow decreased in control subjects during stage II of VM. This was associated with increased splanchnic blood volume, decreased thoracic blood volume, increased heart rate, and decreased blood pressure in POTS. Pelvic and leg resistances were increased above control and remained so during stage IV of VM, accounting for the increased blood pressure overshoot in POTS. Thus splanchnic hyperemia and hypervolemia are related to excessive phase II blood pressure reduction in POTS despite intense peripheral vasoconstriction. Factors other than autonomic dysfunction may play a role in POTS.


1961 ◽  
Vol 201 (1) ◽  
pp. 109-111 ◽  
Author(s):  
Noel M. Bass ◽  
Vincent V. Glaviano

Heart rate, mean blood pressure, adrenal blood flow, and adrenal plasma adrenaline and noradrenaline were compared before and after ligation of the anterior descending coronary artery in dogs anesthetized with chloralose. One group of 12 dogs responded to acute coronary occlusion with a sudden and marked decrease in mean blood pressure (mean, 31%) and heart rate (mean, 18%) followed by an early onset (mean, 227 sec) of ventricular fibrillation. Another group of nine dogs responded with slight decreases in mean blood pressure (mean, 13%) and heart rate (mean, 5%), during which time ventricular fibrillation occurred late (mean, 30 min) or not at all. While the two groups were statistically different in mean blood pressure and heart rate, the minute output of adrenal catecholamines in either group was not found to be related to the early or late occurrence of ventricular fibrillation.


Author(s):  
Alex Buoite Stella ◽  
Giovanni Furlanis ◽  
Nicolò Arjuna Frezza ◽  
Romina Valentinotti ◽  
Milos Ajcevic ◽  
...  

AbstractThe autonomic nervous system (ANS) can be affected by COVID-19, and dysautonomia may be a possible complication in post-COVID individuals. Orthostatic hypotension (OH) and postural tachycardia syndrome (POTS) have been suggested to be common after SARS-CoV-2 infection, but other components of ANS function may be also impaired. The Composite Autonomic Symptom Scale 31 (COMPASS-31) questionnaire is a simple and validated tool to assess dysautonomic symptoms. The aim of the present study was to administer the COMPASS-31 questionnaire to a sample of post-COVID patients with and without neurological complaints. Participants were recruited among the post-COVID ambulatory services for follow-up evaluation between 4 weeks and 9 months from COVID-19 symptoms onset. Participants were asked to complete the COMPASS-31 questionnaire referring to the period after COVID-19 disease. Heart rate and blood pressure were manually taken during an active stand test for OH and POTS diagnosis. One-hundred and eighty participants were included in the analysis (70.6% females, 51 ± 13 years), and OH was found in 13.8% of the subjects. Median COMPASS-31 score was 17.6 (6.9–31.4), with the most affected domains being orthostatic intolerance, sudomotor, gastrointestinal and pupillomotor dysfunction. A higher COMPASS-31 score was found in those with neurological symptoms (p < 0.01), due to more severe orthostatic intolerance symptoms (p < 0.01), although gastrointestinal (p < 0.01), urinary (p < 0.01), and pupillomotor (p < 0.01) domains were more represented in the non-neurological symptoms group. This study confirms the importance of monitoring ANS symptoms as a possible complication of COVID-19 disease that may persist in the post-acute period.


2008 ◽  
Vol 294 (2) ◽  
pp. F309-F315 ◽  
Author(s):  
Joo Lee Cham ◽  
Emilio Badoer

Redistribution of blood from the viscera to the peripheral vasculature is the major cardiovascular response designed to restore thermoregulatory homeostasis after an elevation in body core temperature. In this study, we investigated the role of the hypothalamic paraventricular nucleus (PVN) in the reflex decrease in renal blood flow that is induced by hyperthermia, as this brain region is known to play a key role in renal function and may contribute to the central pathways underlying thermoregulatory responses. In anesthetized rats, blood pressure, heart rate, renal blood flow, and tail skin temperature were recorded in response to elevating body core temperature. In the control group, saline was microinjected bilaterally into the PVN; in the second group, muscimol (1 nmol in 100 nl per side) was microinjected to inhibit neuronal activity in the PVN; and in a third group, muscimol was microinjected outside the PVN. Compared with control, microinjection of muscimol into the PVN did not significantly affect the blood pressure or heart rate responses. However, the normal reflex reduction in renal blood flow observed in response to hyperthermia in the control group (∼70% from a resting level of 11.5 ml/min) was abolished by the microinjection of muscimol into the PVN (maximum reduction of 8% from a resting of 9.1 ml/min). This effect was specific to the PVN since microinjection of muscimol outside the PVN did not prevent the normal renal blood flow response. The data suggest that the PVN plays an essential role in the reflex decrease in renal blood flow elicited by hyperthermia.


1963 ◽  
Vol 18 (5) ◽  
pp. 987-990 ◽  
Author(s):  
Shanker Rao

Reports of cardiovascular responses to head-stand posture are lacking in literature. The results of the various responses, respectively, to the supine, erect, and head-stand posture, are as follows: heart rate/min 67, 84, and 69; brachial arterial pressure mm Hg 92, 90, and 108; posterior tibial arterial pressure mm Hg 98, 196, and 10; finger blood flow ml/100 ml min 4.5, 4.4, and 5.2; toe blood flow ml/100 ml min 7.1, 8.1, and 3.4; forehead skin temperature C 34.4, 34.0 and 34.3; dorsum foot skin temperature C 28.6, 28.2, and 28.2. It is inferred that the high-pressure-capacity vessels between the heart level and posterior tibial artery have little nervous control. The high-pressure baroreceptors take active part in postural adjustments of circulation. The blood pressure equating mechanism is not as efficient when vital tissues are pooled with blood as when blood supply to them is reduced. man; heart rate; blood flow; skin temperature Submitted on January 3, 1963


Entropy ◽  
2018 ◽  
Vol 20 (11) ◽  
pp. 860 ◽  
Author(s):  
Marcos Hortelano ◽  
Richard Reilly ◽  
Francisco Castells ◽  
Raquel Cervigón

Orthostatic intolerance syndrome occurs when the autonomic nervous system is incapacitated and fails to respond to the demands associated with the upright position. Assessing this syndrome among the elderly population is important in order to prevent falls. However, this problem is still challenging. The goal of this work was to determine the relationship between orthostatic intolerance (OI) and the cardiovascular response to exercise from the analysis of heart rate and blood pressure. More specifically, the behavior of these cardiovascular variables was evaluated in terms of refined composite multiscale fuzzy entropy (RCMFE), measured at different scales. The dataset was composed by 65 older subjects, 44.6% (n = 29) were OI symptomatic and 55.4% (n = 36) were not. Insignificant differences were found in age and gender between symptomatic and asymptomatic OI participants. When heart rate was evaluated, higher differences between groups were observed during the recovery period immediately after exercise. With respect to the blood pressure and other hemodynamic parameters, most significant results were obtained in the post-exercise stage. In any case, the symptomatic OI group exhibited higher irregularity in the measured parameters, as higher RCMFE levels in all time scales were obtained. This information could be very helpful for a better understanding of cardiovascular instability, as well as to recognize risk factors for falls and impairment of functional status.


2018 ◽  
Vol 115 (3) ◽  
pp. 590-601 ◽  
Author(s):  
Dino Premilovac ◽  
Emily Attrill ◽  
Stephen Rattigan ◽  
Stephen M Richards ◽  
Jeonga Kim ◽  
...  

Abstract Aims Angiotensin II (AngII) is a potent vasoconstrictor implicated in both hypertension and insulin resistance. Insulin dilates the vasculature in skeletal muscle to increase microvascular blood flow and enhance glucose disposal. In the present study, we investigated whether acute AngII infusion interferes with insulin’s microvascular and metabolic actions in skeletal muscle. Methods and results Adult, male Sprague-Dawley rats received a systemic infusion of either saline, AngII, insulin (hyperinsulinaemic euglycaemic clamp), or insulin (hyperinsulinaemic euglycaemic clamp) plus AngII. A final, separate group of rats received an acute local infusion of AngII into a single hindleg during systemic insulin (hyperinsulinaemic euglycaemic clamp) infusion. In all animals’ systemic metabolic effects, central haemodynamics, femoral artery blood flow, microvascular blood flow, and skeletal muscle glucose uptake (isotopic glucose) were monitored. Systemic AngII infusion increased blood pressure, decreased heart rate, and markedly increased circulating glucose and insulin concentrations. Systemic infusion of AngII during hyperinsulinaemic euglycaemic clamp inhibited insulin-mediated suppression of hepatic glucose output and insulin-stimulated microvascular blood flow in skeletal muscle but did not alter insulin’s effects on the femoral artery or muscle glucose uptake. Local AngII infusion did not alter blood pressure, heart rate, or circulating glucose and insulin. However, local AngII inhibited insulin-stimulated microvascular blood flow, and this was accompanied by reduced skeletal muscle glucose uptake. Conclusions Acute infusion of AngII significantly alters basal haemodynamic and metabolic homeostasis in rats. Both local and systemic AngII infusion attenuated insulin’s microvascular actions in skeletal muscle, but only local AngII infusion led to reduced insulin-stimulated muscle glucose uptake. While increased local, tissue production of AngII may be a factor that couples microvascular insulin resistance and hypertension, additional studies are needed to determine the molecular mechanisms responsible for these vascular defects.


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