Cardiovascular Reflex Responses in Patients with Unexplained Syncope

1989 ◽  
Vol 77 (5) ◽  
pp. 547-553 ◽  
Author(s):  
M. M. A. E. Wahbha ◽  
C. A. Morley ◽  
Y. M. H. Al-Shamma ◽  
R. Hainsworth
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Postural Hypotension ◽  
Vasovagal Syncope ◽  
Pulse Interval ◽  
Reflex Responses ◽  
Non Invasive ◽  
Control Subjects ◽  
Cardiovascular Reflex ◽  
Age Related

1. This study was undertaken to determine whether, in a group of patients complaining of recurrent syncopal attacks but with no apparent cause, there was evidence of abnormal cardiovascular reflex control. 2. The steady-state responses of blood pressure, heart rate and cardiac output to head-up tilting were determined in 67 patients using entirely ‘non-invasive’ methods. In some patients we also studied the immediate response of pulse interval to carotid baroreceptor stimulation by neck suction. 3. Two of the patients developed vasovagal attacks during the 20 min test period of head-up tilting. Eighteen others showed postural hypotension, defined as a fall in blood pressure to outside the limits of two sds from the mean values of age-related control subjects. 4. Patients who showed postural hypotension had a mean fall in cardiac output significantly larger than that in age-related control subjects. Responses in the non-hypotensive patients did not differ significantly from controls. 5. Stimulation of carotid baroreceptors resulted in significantly smaller responses of pulse interval in the patients defined as having postural hypotension compared with the non-hypotensive patients and with the age-related control subjects. 6. In some of the patients who did not show postural hypotension during the standard test, the duration of tilt was prolonged for up to 1 h. Five out of 26 patients developed vasovagal attacks. All the vasovagal patients showed an initial tachycardia and the response of pulse interval to neck suction was significantly larger than in the controls. 7. This study has shown that simple non-invasive tests of cardiovascular reflex function can divide patients with poor orthostatic tolerance into two groups: those with evidence of small reflex responses, associated with abnormally large falls in cardiac output during tilting, and those with evidence of overactive reflexes associated with the tendency to develop vasovagal syncope.

scholarly journals Disruption of phase synchronization between blood pressure and muscle sympathetic nerve activity in postural vasovagal syncope

2013 ◽  
Vol 305 (8) ◽  
pp. H1238-H1245 ◽  
Author(s):  
Christopher E. Schwartz ◽  
Elisabeth Lambert ◽  
Marvin S. Medow ◽  
Julian M. Stewart
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Phase Synchronization ◽  
Vasovagal Syncope ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Control Subjects ◽  
Late Stages

Withdrawal of muscle sympathetic nerve activity (MSNA) may not be necessary for the precipitous fall of peripheral arterial resistance and arterial pressure (AP) during vasovagal syncope (VVS). We tested the hypothesis that the MSNA-AP baroreflex entrainment is disrupted before VVS regardless of MSNA withdrawal using the phase synchronization between blood pressure and MSNA during head-up tilt (HUT) to measure reflex coupling. We studied eight VVS subjects and eight healthy control subjects. Heart rate, AP, and MSNA were measured during supine baseline and at early, mid, late, and syncope stages of HUT. Phase synchronization indexes, measuring time-dependent differences between MSNA and AP phases, were computed. Directionality indexes, indicating the influence of AP on MSNA (neural arc) and MSNA on AP (peripheral arc), were computed. Heart rate was greater in VVS compared with control subjects during early, mid, and late stages of HUT and significantly declined at syncope ( P = 0.04). AP significantly decreased during mid, late, and syncope stages of tilt in VVS subjects only ( P = 0.001). MSNA was not significantly different between groups during HUT ( P = 0.700). However, the phase synchronization index significantly decreased during mid and late stages in VVS subjects but not in control subjects ( P < .001). In addition, the neural arc was significantly affected more than the peripheral arc before syncope. In conclusion, VVS is accompanied by a loss of the synchronous AP-MSNA relationship with or without a loss in MSNA at faint. This provides insight into the mechanisms behind the loss of vasoconstriction and drop in AP independent of MSNA at the time of vasovagal faint.

Non-Invasive Monitoring of Hemodynamic Parameters during Hemodialysis

1995 ◽  
Vol 18 (9) ◽  
pp. 499-503 ◽  
Author(s):  
F. Pizzarelli ◽  
P. Dattolo ◽  
M. Piacenti ◽  
M.A. Morales ◽  
T. Cerrai ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Blood Volume ◽  
Impedance Cardiography ◽  
Hemodynamic Parameters ◽  
Non Invasive ◽  
Transthoracic Impedance ◽  
Cardiac Output Index ◽  
On Line ◽  
Two Parameters

We studied in 13 hemodialysis patients intradialytic variations of blood volume (BV) and cardiac output, by means of non-invasive methods. We found a weak correlation, r 0.2 or less, between BV variations and intradialysis blood pressure variations. The sensitivity of the former in describing the variations of the latter was only 32%. During the 30 min preceeding the hypotensive crisis the percent BV variations did not show any predictive trend. On the contrary, refilling increased as blood pressure dropped and a weak inverse relation (r -0.35) was found between these two parameters. Unstable patients had predialytic blood volume values significantly lower than stable ones and comparable to healthy subjects. On the contrary, the correlation between percent variations of cardiac output index and MAP was 0.68 with a sensitivity and specificity of 90% and 59%, respectively. Unfortunately these promising results were obtained only with an estimate of cardiac output obtained by echocardiography and not by transthoracic impedance cardiography, which is much more feasible than the former as on-line monitoring of cardiac output. On-line monitoring of hemodynamic parameters is an appealing but still unsolved task.

Is neurocardiovascular instability a risk factor for cognitive decline and/or dementia? The science to date

2007 ◽  
Vol 17 (3) ◽  
pp. 153-160 ◽  
Author(s):  
Orla Collins ◽  
Rose Anne Kenny
Keyword(s):  
Blood Pressure ◽  
Older People ◽  
Carotid Sinus ◽  
Vasovagal Syncope ◽  
Hypersensitivity Syndrome ◽  
Age Related ◽  
Co Morbidity ◽  
Criteria For Diagnosis ◽  
Rate Behaviour ◽  
Humoral Control

Neurocardiovascular instability (NCVI) is defined as ‘age-related changes in blood pressure and heart-rate behaviour, predominantly resulting in hypotension and bradyarrhythmia’ The four most common presentations of NCVI are orthostatic hypotension (OH), carotid sinus hypersensitivity/syndrome (CSH/CSS), vasovagal syncope (VVS) and post-prandial hypotension (PPH), although there is considerable overlap between these conditions. The criteria for diagnosis of these syndromes are given in Table 1. Clinically, these conditions manifest as dizziness, falls, pre-syncope and syncope. Older people are more susceptible to NCVI because of age-related physiological changes in the cardiovascular system, the autonomic nervous system, and humoral control of blood pressure. These neurocardiovascular changes are further complicated by co-morbidity and polypharmacy in older people.

Systemic hemodynamic determinants of blood pressure in women: age, physical activity, and hormone replacement

1997 ◽  
Vol 273 (2) ◽  
pp. H777-H785 ◽  
Author(s):  
B. E. Hunt ◽  
K. P. Davy ◽  
P. P. Jones ◽  
C. A. DeSouza ◽  
R. E. Van Pelt ◽  
...  
Keyword(s):  
Physical Activity ◽  
Blood Pressure ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Hormone Replacement ◽  
Systemic Hemodynamic ◽  
Arterial Blood ◽  
Age Related ◽  
Hemodynamic Determinants

We tested the hypothesis that the age-related changes in systemic hemodynamic determinants of arterial blood pressure in healthy women are related to physical activity and hormone replacement status. We studied 66 healthy, normotensive premenopausal (21-35 yr) and postmenopausal (50-72 yr) sedentary and endurance-trained women under supine resting conditions. Mean blood pressure was 7 mmHg higher in sedentary post- compared with premenopausal women, which was associated with an 11-mmHg higher systolic blood pressure, a 25% lower stroke volume and cardiac output, and a 50% higher systemic vascular resistance (all P < 0.05). Absolute (ml) levels of total blood volume did not differ across age, but resting oxygen consumption was approximately 35% lower in the postmenopausal women (P < 0.05). The elevations in mean and systolic blood pressures with age were similar in endurance-trained runners, but, in contrast to the sedentary women, the elevations were not associated with significant age-related differences in cardiac output, stroke volume, or oxygen consumption, and only a modest (15%) increase in systemic vascular resistance (P = 0.06). Postmenopausal swimmers demonstrated the same systemic hemodynamic profile as that of postmenopausal runners, indicating a nonspecific influence of the endurance-trained state. Blood pressure and its systemic hemodynamic determinants did not differ in postmenopausal users compared with those of nonusers of hormone replacement therapy. Resting oxygen consumption was the strongest physiological correlate of cardiac output in the overall population (r = 0.65, P < 0.001). We conclude that 1) the increases in arterial blood pressure at rest with age in healthy normotensive women are not obviously related to habitual physical activity status; 2) the systemic hemodynamic determinants of the age-related elevations in blood pressure are fundamentally different in sedentary vs. active women, possibly due, in part, to an absence of decline in resting oxygen consumption in the latter; and 3) systemic hemodynamics at rest are not different in healthy normotensive postmenopausal users vs. nonusers of estrogen-based hormone replacement.

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.

scholarly journals Non-invasive evaluation of cerebral hemodynamic and intracranial pressure in pediatric neuroinfections

2018 ◽  
Vol 9 (4) ◽  
pp. 485-490
Author(s):  
М. А. Georgiynts ◽  
V. А. Коrsunov ◽  
О. М. Оlkhovska ◽  
К. E. Stoliarov
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Intensive Care ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Flow Index ◽  
Non Invasive ◽  
Group I ◽  
Group Ii

The study of intracranial pressure (eICP), cerebral perfusion pressure (eCPP), cerebral blood flow index (CFI), zero flow pressure (ZFP) in 49 children hospitalized in the intensive care unit with severe course of neuroinfections was carried out. The level of consciousness was determined by the Glasgow pediatric scale. Monitoring of central and peripheral hemodynamics (ECG, heart rate, systolic, diastolic and mean blood pressure, and cardiac output), pulse oximetry, capnography, hemoglobin, hematocrit, total protein, urea, creatinine, lactate, glucose and serum electrolytes was done. An ultrasound scanner was used to perform ultrasound duplex scanning of blood flow in the left and middle cerebral artery (MCA), measuring maximum, minimum and average blood flow velocities, pulsation index (PI), and resistance index (RI). Based on the formulae of Edouard et al. indicators of eCPP, ZFP, CFI, eICP were calculated. The eSCP was also determined by the formulae of Kligenchöfer et al. and Bellner et al. All patients were divided into group I with RI > 1.3 and group II with RI < 1.3. It was found that eCPP in the group I was significantly less (29.5 ± 1.3 mm Hg) than in the II group (41.6 ± 1.7 mm Hg). Despite the lack of a reliable difference in blood pressure between groups I and II, the difference in eCPP was found due to a significant difference in eICP 34.6 ± 1.4 and 27.6 ± 0.89 mm Hg in I and II groups respectively. ZFP in group I was significantly higher than in group II. The indexes of the Glasgow coma scale was significantly lower in group I and 7.8 ± 0.6 points. There were observed direct moderate correlations between systolic blood pressure, cardiac output and eSRP and CFI, presumably associated with a loss of autoregulation. CFI in the group I was lower than in the group II. Thus, non-invasive examination of cerebral flow in MCA by duplex sonography revealed that PI > 1.3 is an informative marker of intracranial hypertension and reduction of cerebral perfusion, which is common in children with neuroinfections. To determine the eSRP and CFI it is advisable to use the formula of Edouard et al. and to determine the eICP the formula of Kligenchöfer et al. The obtained data can be useful for objectifying the severity of the condition, predicting the outcomes of neuroinfections, choosing the directions of intensive care and evaluating its effectiveness.

Decrease in cardiac output and muscle sympathetic activity during vasovagal syncope

2002 ◽  
Vol 282 (5) ◽  
pp. H1804-H1809 ◽  
Author(s):  
D. L. Jardine ◽  
I. C. Melton ◽  
I. G. Crozier ◽  
S. English ◽  
S. I. Bennett ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Sympathetic Nerve Activity ◽  
Vasovagal Syncope ◽  
Peripheral Resistance ◽  
Blood Pressure Level ◽  
Progressive Decline ◽  
Vasovagal Reactions ◽  
Head Up Tilt ◽  
Regression Slopes

The importance of cardiac output (CO) to blood pressure level during vasovagal syncope is unknown. We measured thermodilution CO, mean blood pressure (MBP), and leg muscle mean sympathetic nerve activity (MSNA) each minute during 60° head-up tilt in 26 patients with recurrent syncope. Eight patients tolerated tilt (TT) for 45 min (mean age 60 ± 5 yr) and 15 patients developed syncope during tilt (TS) (mean age 58 ± 4 yr, mean tilt time 15.4 ± 2 min). In TT patients, CO decreased during the first minute of tilt (from 3.2 ± 0.2 to 2.5 ± 0.3 l · min−1 · m−2, P = 0.001) and thereafter remained stable between 2.5 ± 0.3 ( P = 0.001) and 2.4 ± 0.2 l · min−1 · m−2( P = 0.004) at 5 and 45 min, respectively. In TS patients, CO decreased during the first minute (from 3.3 ± 0.2 to 2.7 ± 0.1 l · min−1 · m−2, P = 0.02) and was stable until 7 min before syncope, falling to 2.0 ± 0.2 at syncope ( P = 0.001). Regression slopes for CO versus time during tilt were −0.01 min−1 in TT versus −0.1 l · min−1 · m−2 · min−1in TS ( P = 0.001). However, MBP was more closely correlated to total peripheral resistance ( R = 0.56, P = 0.001) and MSNA ( R = 0.58, P = 0.001) than CO ( R = 0.32, P = 0.001). In vasovagal reactions, a progressive decline in CO may contribute to hypotension some minutes before syncope occurs.

Maternal hemodynamics during labor epidural analgesia with and without adrenaline: a secondary analysis of a randomized trial

2020 ◽  
Author(s):  
Felix Haidl ◽  
Christian Tronstad ◽  
Leiv Arne Rosseland ◽  
Vegard Dahl
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Epidural Analgesia ◽  
Systolic Blood Pressure ◽  
Secondary Analysis ◽  
Uterine Contractions ◽  
Non Invasive ◽  
Enhance Efficiency ◽  
Labor Epidural

Abstract Background: Pregnancy in general and labor in particular is associated with changes in maternal hemodynamic parameters such as increased cardiac output and heart rate, with peaks during uterine contractions. Adrenaline may be added to labor epidural solutions to enhance efficiency, but the hemodynamic fluctuations may increase. The aim of this study was to compare the hemodynamic changes of epidural drug solution with or without adrenaline 2 µg.ml -1 and to provide pilot data for a larger study. Methods: Forty-one nulliparous laboring women requesting epidural analgesia were randomized to epidural solution of bupivacaine 1mg.ml -1 , fentanyl 2 µg.ml -1 with or without adrenaline 2 µg.ml -1 . The participants were monitored with the Nexfin CC continuous non-invasive blood pressure and cardiac output monitor. The primary outcomes were changes in peak systolic blood pressure and cardiac output at uterine contraction within 30 minutes after epidural activation. The effect of adrenaline was tested statistically by a linear mixed effects model of the outcome variables’ dependency on time, adrenaline and their interaction. Results: The addition of adrenaline to the solution had no statistically significant effect on the temporal changes in peak systolic blood pressure (mean change 0.23 mmHg.min -1 95% CI [-0.17; 0.64] p=0.26), peak cardiac output (mean change 0.0029 l.min -1 .min -1 95 % CI [-0.026; 0.032] 0.84), or heart rate (mean change 0.015 beats.min -1 .min -1 95 % CI [-0.25; 0.28] p=0.91).

Afferent baroreflex dysfunction and age-related orthostatic hypotension

1991 ◽  
Vol 81 (s25) ◽  
pp. 531-538 ◽  
Author(s):  
A. L. Tonkin ◽  
L. M. H. Wing ◽  
M. J. Morris ◽  
V. Kapoor
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cold Stress ◽  
Orthostatic Hypotension ◽  
Autonomic Neuropathy ◽  
Isometric Exercise ◽  
Control Subjects ◽  
Age Related ◽  
Head Up Tilt ◽  
Elderly Control

1. To test the hypothesis that in apparently healthy elderly subjects with orthostatic hypotension there is afferent baroreflex dysfunction, cardiovascular and neurohumoral responses were measured after separate stimuli which activated baroreceptor (head-up tilt) and non-baroreceptor (cold stress, isometric exercise) afferent pathways. 2. In 15 healthy elderly control subjects blood pressure did not change with 60° head-up tilting and there was a moderate increase in heart rate, whereas in 13 subjects with age-related orthostatic hypotension head-up tilting was associated with a marked fall in blood pressure but a similar heart rate response to that in the elderly control group. In contrast, both groups of subjects had similar blood pressure and heart rate responses to cold stress and sustained isometric exercise. 3. Nine subjects with autonomic neuropathy also showed a marked hypotensive response to head-up tilt, but produced no pressor response to cold stress or isometric exercise. 4. The plasma concentrations of noradrenaline, adrenaline and neuropeptide-Y-like immunoreactivity rose and that of atrial natriuretic peptide fell after head-up tilt in the study population as a whole. There were no significant differences between groups despite the much greater blood pressure drops in the subjects with autonomic neuropathy and in those with age-associated orthostatic hypotension. 5. The aorto-iliac pulse wave velocity index was significantly higher in subjects with age-associated orthostatic hypotension compared with that in control subjects. 6. The pattern of responses to the separate stresses observed in the group with age-associated orthostatic hypotension is characteristic and different from that in the elderly control subjects and the subjects with autonomic neuropathy. It suggests that age-associated orthostatic hypotension is related predominantly to dysfunction in the afferent limb of the baroreflex arc, possibly partially caused by a splinting of arterial baroreceptors by non-compliant arterial walls.

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