Mechanisms underlying the impairment in orthostatic tolerance after nocturnal recumbency in patients with autonomic failure

2001 ◽  
Vol 101 (6) ◽  
pp. 609-618 ◽  
Author(s):  
Stefano OMBONI ◽  
Adrianus A.J. SMIT ◽  
Johannes J. VAN LIESHOUT ◽  
Jos J. SETTELS ◽  
Gerard J. LANGEWOUTERS ◽  
...  

In the present study, we have assessed in patients with neurogenic orthostatic hypotension the haemodynamics underlying the reduced tolerance to standing after prolonged recumbency at night. In 10 patients with neurogenic orthostatic hypotension (age 33-68 years), of which seven were being treated with fludrocortisone and/or sleeping in the 12° head-up tilt position, 24h continuous non-invasive finger blood pressure was recorded by a Portapres device. Beat-to-beat blood pressure, heart rate, stroke volume, cardiac output and total peripheral vascular resistance obtained by pulse contour analysis were assessed during 5min of standing in the evening (at 22.30 hours) and in the morning (at 06.30hours). On average, the inverse of the normal 24h blood pressure profile was found, with a large diversity in blood pressure profiles among patients. Supine blood pressure values were similar, but standing blood pressure values were lower in the morning than in the evening (P < 0.01). This resulted from larger falls in stroke volume and cardiac output upon standing in the morning compared with the evening, while total peripheral resistance did not change. There was no relationship between the decrease in body weight during the night (mean 0.9kg; range 0.2-1.6kg) and the evening-morning difference in standing blood pressure. We conclude that, in patients with neurogenic orthostatic hypotension, the impaired tolerance to standing in the morning is due to larger falls in stroke volume and cardiac output. Not only nocturnal polyuria, but also a redistribution of body fluid, are likely mechanisms underlying the pronounced decreases in stroke volume and cardiac output after prolonged recumbency at night.

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

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.


1988 ◽  
Vol 254 (4) ◽  
pp. H811-H815 ◽  
Author(s):  
D. G. Parkes ◽  
J. P. Coghlan ◽  
J. G. McDougall ◽  
B. A. Scoggins

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.


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.


2020 ◽  
Vol 14 ◽  
pp. 117954682095341
Author(s):  
Dinesh K Kalra ◽  
Anvi Raina ◽  
Sumit Sohal

Neurogenic orthostatic hypotension (nOH) is a subtype of orthostatic hypotension in which patients have impaired regulation of standing blood pressure due to autonomic dysfunction. Several primary and secondary causes of this disease exist. Patients may present with an array of symptoms making diagnosis difficult. This review article addresses the epidemiology, pathophysiology, causes, clinical features, and management of nOH. We highlight various pharmacological and non-pharmacological approaches to treatment, and review the recent guidelines and our approach to nOH.


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.


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.


1987 ◽  
Vol 63 (1) ◽  
pp. 270-276 ◽  
Author(s):  
J. M. Hagberg ◽  
S. J. Montain ◽  
W. H. Martin

Recently, systolic and diastolic blood pressure have been reported to be significantly lower for several hours after exercise than when measured at rest before exercise in individuals with essential hypertension. We sought to determine the hemodynamic mechanism underlying this reduction in blood pressure. Twenty-four men and women 60–69 yr of age with persistent essential hypertension completed one of the following protocols: exercise at 50% of maximum O2 consumption (VO2 max) followed by 1 h of recovery, exercise at 70% of VO2 max followed by 3 h of recovery, or a 4-h control study. Systolic pressure was significantly lower during recovery after both intensities of exercise, but diastolic pressure was unchanged. The lower blood pressure was primarily due to a reduction in cardiac output, since total peripheral resistance was increased throughout both recovery periods. Cardiac output was reduced in recovery because of a reduction in stroke volume. Heart rate was above, or no different from, that at rest before exercise. Changes in plasma volume could not entirely account for the reduction in stroke volume. Therefore, other mechanisms altering venous return and/or myocardial contractility appear to be responsible for the reduction in systolic blood pressure evident after a single bout of submaximal exercise in individuals with essential hypertension.


Author(s):  
Horacio Kaufmann ◽  
Ross Vickery ◽  
Whedy Wang ◽  
Jitendra Kanodia ◽  
Cyndya A. Shibao ◽  
...  

Abstract Purpose In neurogenic orthostatic hypotension, blood pressure falls when upright owing to impaired release of norepinephrine, leading to dizziness. Ampreloxetine, a selective norepinephrine reuptake inhibitor, increases circulating norepinephrine levels. This study explored the safety of ampreloxetine and its effect on blood pressure and symptoms in patients with neurogenic orthostatic hypotension. Methods A multicenter ascending-dose trial (range 1–20 mg, Part A) was followed by a 1 day, double-blind, randomized, placebo-controlled study (median dose 15 mg, Part B). Eligible patients then enrolled in a 20-week, open-label, steady-state extension phase (median dose 10 mg, Part C) followed by a 4-week withdrawal. Assessments included the Orthostatic Hypotension Symptom Assessment Scale (item 1), supine/seated/standing blood pressure, and safety. Results Thirty-four patients (age 66 ± 8 years, 22 men) were enrolled. Part A: The proportion of participants with a positive response (i.e., increase from baseline in seated systolic blood pressure of ≥ 10 mmHg) was greater with the 5 and 10 mg ampreloxetine doses than with placebo or other active ampreloxetine doses. Part B: Seated blood pressure increased 15.7 mmHg 4 h after ampreloxetine and decreased 14.2 mmHg after placebo [least squares mean difference (95% CI) 29.9 mmHg (7.6–52.3); P = 0.0112]. Part C: Symptoms of dizziness/lightheadedness improved 3.1 ± 3.0 points from baseline and standing systolic blood pressure increased 11 ± 12 mmHg. After 4 weeks of withdrawal, symptoms returned to pretreatment levels. The effect of ampreloxetine on supine blood pressure was minimal throughout treatment duration. Conclusion Ampreloxetine was well tolerated and improved orthostatic symptoms and seated/standing blood pressure with little change in supine blood pressure. Trial registration NCT02705755 (first posted March 10, 2016).


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