Hypotension induced by passive head-up tilt: endocrine and circulatory mechanisms

Sander‐Jensen, K.; Secher, Niels H.; Astrup, A; Christensen, N. J.; Giese, J.; Schwartz, T. W.; Warberg, Jørgen; Bie, Peter

doi:10.1152/ajpregu.1986.251.4.r742

Cited by 102 publications

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“…3 In addition, it has been observed that the administration of exogenous catecholamines 4 or nitroglycerin 5 before a tilt test promotes neurogenic fainting in susceptible subjects by eliciting a direct or reflex increase in sympathetic activity.…”

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confidence: 99%

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Cardiac Autonomic Patterns Preceding Occasional Vasovagal Reactions in Healthy Humans

et al. 1998

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Background-The wide range of clinical presentation of orthostatic vasovagal syncope suggests different underlying changes in the cardiac autonomic modulation. Methods and Results-To evaluate the beat-by-beat modifications in the neural control of heart period preceding a syncopal event, we studied RR interval variability in 22 healthy subjects who experienced fainting for the first time during a 90°head-up tilt and in 22 control subjects by means of time-variant power spectral analysis. Sympathetic and vagal modulations to the sinoatrial node were assessed by the normalized power of the low-frequency (LF, Ϸ0.1-Hz) and high-frequency (HF, Ϸ0.25-Hz) oscillatory components of RR variability. When the patients were supine, no differences were observed in the hemodynamic and spectral parameters of the 2 groups. During the tilt procedure, RR, LF NU , and HF NU (NUϭnormalized units) values were relatively stable in control subjects. During early tilt (T 1 ), subjects with syncope had reduced RR intervals compared with control subjects. In 13 subjects with syncope, RR decreased while LF NU and LF/HF increased in the last minute of tilt before syncope (T 2 ). Conversely, in the remaining 9 fainters, LF NU and LF/HF decreased from T 1 to T 2 and HF NU increased slightly. Conclusions-Two different patterns may be recognized in the cardiac autonomic changes preceding an occasional vasovagal event, namely, one characterized by a progressive increase of the marker of cardiac sympathetic modulation up to the onset of syncope, the other by a sympathetic inhibition with an impending vagal predominance. The recognition of different pathophysiological mechanisms in fainters may have important therapeutic implications.

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“…For instance, plasma norepinephrine concentrations have been found to be elevated 3,6 or diminished 7,8 before syncope. Studies based on conventional power spectral analysis of RR variability have indicated increased, 9,10 reduced, 11,12 or unchanged 13 values of the markers of cardiac sympathetic modulation before a vasovagal event.…”

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confidence: 99%

Cardiac Autonomic Patterns Preceding Occasional Vasovagal Reactions in Healthy Humans

et al. 1998

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“…The main receptors involved in these adjustments are the cardiopulmonary mechanoreceptors, located at the level of the right atrium and the pulmonary veins, and the sinoaortic receptors, located in the carotid sinus and aortic arch 38 . In addition to responding, in an isolated form, for the alterations in circulatory volume, these baroreceptors present a complex inhibitory interaction between the cardiopulmonary and the sinoaortic barorefl exes, which causes the reduction in the cardiopulmonary afferent input to increase the gain of sinoaortic barorefl ex 39 .…”

Section: The Orthostatic Posturementioning

confidence: 99%

“…From a functional point of view, the two components of the arterial barorefl ex (carotid and aortic) are not equivalent. It has been suggested that the aortic barorefl ex has a higher threshold and lower sensitivity than the carotid one 38 . The information of the baroreceptors is transmitted through several pathways that accompany the route of the ninth and tenth cranial pairs until the brainstem centers.…”

Section: The Orthostatic Posturementioning

confidence: 99%

Contribuição dos grandes vasos arteriais na adaptação cardiovascular a ortostase

Neto¹

2006

Arq. Bras. Cardiol.

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“…Examples of these include markedly elevated epinephrine, vasopressin, ␤-endorphins, and pancreatic polypeptide levels and altered baroreceptor sensitivity in the faint-prone individual. 50,51 Such differences (among many others of which we are as yet unaware) may impact the capability of the central nervous system to protect circulatory stability. In this regard, ␤-endorphin levels are increased in both vasovagal syncope and the analogous second stage of hemorrhagic shock.…”

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confidence: 99%

Pharmacotherapy of Neurally Mediated Syncope

et al. 1999

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Abstract-A wide variety of pharmacological agents are currently used for prevention of recurrent neurally mediated syncope, especially the vasovagal faint. None, however, have unequivocally proven long-term effectiveness based on adequate randomized clinical trials. At the present time, ␤-adrenergic receptor blockade, along with agents that increase central volume (eg, fludrocortisone, electrolyte-containing beverages), appear to be favored treatment options. The antiarrhythmic agent disopyramide and various serotonin reuptake blockers have also been reported to be beneficial. Finally, vasoconstrictor agents such as midodrine offer promise and remain the subject of clinical study. Ultimately, though, detailed study of the pathophysiology of these syncopal disorders and more aggressive pursuit of carefully designed placebo-controlled treatment studies are essential if pharmacological prevention of recurrent neurally mediated syncope is to be placed on a firm foundation. (Circulation. 1999;100:1242-1248.)Key Words: syncope Ⅲ nervous system Ⅲ pharmacology Ⅲ Cardiovascular Drugs N eurally mediated (neurocardiogenic) syncope comprises a number of clinical conditions in which symptomatic systemic hypotension occurs as a result of a transient disturbance of neural reflex cardiovascular control (Table 1). [1][2][3] The vasovagal faint, carotid sinus syndrome, and postmicturition syncope are the most common forms of the neurally mediated faint. Others, including cough syncope and postexertional syncope, are less frequently encountered.This communication focuses on the pharmacological options that have been proposed for preventing neurally mediated faints, and especially the vasovagal faint, because it has been the most thoroughly studied. The objective is to provide an overview of the pharmacology and pertinent proposed modes of action of those agents that may be of benefit. Drug Therapy of Neurally Mediated Syncope: Basic PrinciplesMost individuals who experience a neurally mediated faint (particularly vasovagal fainters) require no additional therapy beyond education (ie, recognition of premonitory symptoms, avoidance of triggering events, and awareness of useful evasive actions) and reassurance regarding the non-lifethreatening nature of the condition. On occasion, stress and anxiety management may be warranted. Various more aggressive nonpharmacological (eg, support hose, extended exposure to upright posture, pacemakers) and pharmacological treatment options are usually reserved for those relatively few individuals who experience frequent syncope and/or when symptoms cause excessive lifestyle difficulties, threaten employment, or result in unacceptable risk of physical injury to the patient or others.Currently, drugs are used for both diagnostic and therapeutic purposes in the patient with neurally mediated syncope. [1][2][3] In terms of diagnostic applications, agents such as isoproterenol, edrophonium, nitroglycerin, and adenosine have been reported to be helpful during tilt-table testing (ie, so-called pharmacolog...

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Hypotension induced by passive head-up tilt: endocrine and circulatory mechanisms

Cited by 102 publications

References 0 publications

Cardiac Autonomic Patterns Preceding Occasional Vasovagal Reactions in Healthy Humans

Cardiac Autonomic Patterns Preceding Occasional Vasovagal Reactions in Healthy Humans

Contribuição dos grandes vasos arteriais na adaptação cardiovascular a ortostase

Pharmacotherapy of Neurally Mediated Syncope

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