Salt supplementation in the management of orthostatic intolerance: Vasovagal syncope and postural orthostatic tachycardia syndrome.

Salt supplementation is a common non-pharmacological approach to the management of recurrent orthostatic syncope or presyncope, particularly for patients with vasovagal syncope (VVS) or postural orthostatic tachycardia syndrome (POTS), although there is limited consensus on the optimal dosage, formulation and duration of treatment. Accordingly, we reviewed the evidence for the use of salt supplementation to reduce susceptibility to syncope or presyncope in patients with VVS and POTS. We found that short-term (~3 months) salt supplementation improves susceptibility to VVS and associated symptoms, with little effect on supine blood pressure. In patients with VVS, salt supplementation is associated with increases in plasma volume, and an increase in the time taken to provoke a syncopal event during orthostatic tolerance testing, with smaller orthostatic heart rate increases, enhanced peripheral vascular responses to orthostatic stress, and improved cerebral autoregulation. Responses were most pronounced in those with a baseline sodium excretion <170 mmol/day. Salt supplementation also improved symptoms, plasma volume, and orthostatic responses in patients with POTS. Salt supplementation should be considered for individuals with recurrent and troublesome episodes of VVS or POTS without cardiovascular comorbidities, particularly if their typical urinary sodium excretion is low, and their supine blood pressure is not elevated. The efficacy of the response, in terms of the improvement in subjective and objective markers of orthostatic intolerance, and any potential deleterious effect on supine blood pressure, should be routinely monitored in individuals on high salt regimes.

A practical guide to active stand testing and analysis using continuous beat-to-beat non-invasive blood pressure monitoring.

PURPOSE: The average adult stands approximately 50-60 times per day. Cardiovascular responses evoked during the first 3 min of active standing provide a simple means to clinically assess short-term neural and cardiovascular function across the lifespan. Clinically, this response is used to identify the haemodynamic correlates of patient symptoms and attributable causes of (pre-)syncope, and to detect autonomic dysfunction, variants of orthostatic hypotension, postural orthostatic tachycardia syndrome and orthostatic hypertension. METHODS: This paper provides a set of experience/expertise-based recommendations detailing current state-of-the-art measurement and analysis approaches for the active stand test, focusing on beat-to-beat BP technologies. This information is targeted at those interested in performing and interpreting the active stand test to current international standards. RESULTS: This paper presents a practical step-by-step guide on (1) how to perform active stand measurements using beat-to-beat continuous blood pressure measurement technologies, (2) how to conduct an analysis of the active stand response and (3) how to identify the spectrum of abnormal blood pressure and heart rate responses which are of clinical interest. CONCLUSION: Impairments in neurocardiovascular control are an attributable cause of falls and syncope across the lifespan. The simple active stand test provides the clinician with a powerful tool for assessing individuals at risk of such common disorders. However, its simplicity belies the complexity of its interpretation. Care must therefore be taken in administering and interpreting the test in order to maximise its clinical benefit and minimise its misinterpretation.

[Driving status of syncope patients is not part of standard advice]. / Rijgeschiktheid bij syncope niet standaard besproken.

OBJECTIVE: Some medical problems, such as syncope, have direct consequences for fitness to drive. Our objective was to discover if patients had been informed about their driving status after a syncopal episode by their physician, and if this advice was in line with current legislation. DESIGN: Cross-sectional study. METHOD: By means of a structured questionnaire, 150 patients referred to the syncope clinic at the Academic Medical Centre, Amsterdam, were asked about the advice they had received concerning their driving status during previous consultations with their general practitioner or specialists. A syncope expert then assessed the driving status of all patients in the light of the existing and new ruling. RESULTS: In 121 of the 150 patients (81%), a certain or highly-likely cause for their loss of consciousness was determined: 68 patients had reflex syncope, 25 patients orthostatic hypotension, 20 patients psychogenic pseudosyncope, three patients cardiac syncope, three patients had epilepsy and two patients another diagnosis. Seven patients had experienced an episode while driving. Only 26/150 patients (17%) reported that the consequences of their episodes for their driving status had been discussed with them at earlier consultations. If driving was discussed, in only 31% had the current Dutch legislation on driving been followed. Over a third (38%) of the patients felt they should no longer drive. CONCLUSION: Fewer than one in five patients reported that driving status was discussed by a physician after a syncope episode. If advice had been given, it was often not in line with current legislation.

Noninvasive beat-to-beat finger arterial pressure monitoring during orthostasis: a comprehensive review of normal and abnormal responses at different ages.

Over the past 30 years, noninvasive beat-to-beat blood pressure (BP) monitoring has provided great insight into cardiovascular autonomic regulation during standing. Although traditional sphygmomanometric measurement of BP may be sufficient for detection of sustained orthostatic hypotension, it fails to capture the complexity of the underlying dynamic BP and heart rate responses. With the emerging use of noninvasive beat-to-beat BP monitoring for the assessment of orthostatic BP control in clinical and population studies, various definitions for abnormal orthostatic BP patterns have been used. Here, age-related changes in cardiovascular control in healthy subjects will be reviewed to define the spectrum of the most important abnormal orthostatic BP patterns within the first 180 s of standing. Abnormal orthostatic BP responses can be defined as initial orthostatic hypotension (a transient systolic BP fall of >40 mmHg within 15 s of standing), delayed BP recovery (an inability of systolic BP to recover to a value of >20 mmHg below baseline at 30 s after standing) and sustained orthostatic hypotension (a sustained decline in systolic BP of ≥20 mmHg occurring 60-180 s after standing). In the evaluation of patients with light-headedness, pre(syncope), (unexplained) falls or suspected autonomic dysfunction, it is essential to distinguish between normal cardiovascular autonomic regulation and these abnormal orthostatic BP responses. The prevalence, clinical relevance and underlying pathophysiological mechanisms of these patterns differ significantly across the lifespan. Initial orthostatic hypotension is important for identifying causes of syncope in younger adults, whereas delayed BP recovery and sustained orthostatic hypotension are essential for evaluating the risk of falls in older adults.

Initial orthostatic hypotension in teenagers and young adults.

OBJECTIVE: To assess: (1) the frequency of an abnormally large fall in blood pressure (BP) upon standing from supine in patients with initial orthostatic hypotension (IOH); (2) the underlying hemodynamic mechanisms of this fall in BP upon standing from supine and from squatting. METHODS: In a retrospective study of 371 patients (≤30 years) visiting the syncope unit, the hemodynamic response to standing and squatting were studied in 26 patients who were diagnosed clinically with IOH, based on history taking only. In six patients changes in cardiac output (CO) and systemic vascular resistance (SVR) were determined, and the underlying hemodynamics were analyzed. RESULTS: 15/26 (58 %) patients with IOH had an abnormally large initial fall in systolic BP (≥40 mmHg). There was a large scatter in CO and SVR response after arising from supine [ΔCO at BP nadir median -8 % (range -37, +27 %); ΔSVR at BP nadir median -31 % (range -46, +10 %)]. The hemodynamic response after squatting showed a more consistent pattern, with a fall in SVR in all six patients [ΔCO at BP nadir median +23 % (range -12, +31 %); ΔSVR at BP nadir median -42 %, (range -52, -35 %)]. INTERPRETATION: The clinical diagnosis of IOH is based on history taking, as an abnormally large fall in systolic BP can only be documented in 58 %. For IOH upon standing after supine rest, the hemodynamic mechanism can be either a large fall in CO or in SVR. For IOH upon arising from squatting a large fall in SVR is a consistent finding.

At the heart of the arterial baroreflex: a physiological basis for a new classification of carotid sinus hypersensitivity.

The aim of this review is to provide an update of the current knowledge of the physiological mechanisms underlying reflex syncope. Carotid sinus syncope will be used as the classical example of an autonomic reflex with relatively well-established afferent, central and efferent pathways. These pathways, as well as the pathophysiology of carotid sinus hypersensitivity (CSH) and the haemodynamic effects of cardiac standstill and vasodilatation will be discussed. We will demonstrate that continuous recordings of arterial pressure provide a better understanding of the cardiovascular mechanisms mediating arterial hypotension and cerebral hypoperfusion in patients with reflex syncope. Finally we will demonstrate that the current criteria to diagnose CSH are too lenient and that the conventional classification of carotid sinus syncope as cardioinhibitory, mixed and vasodepressor subtypes should be revised because isolated cardioinhibitory CSH (asystole without a fall in arterial pressure) does not occur. Instead, we suggest that all patients with CSH should be thought of as being 'mixed', between cardioinhibition and vasodepression. The proposed stricter set of criteria for CSH should be evaluated in future studies.

MSNA during prolonged post-faint hypotension.

BACKGROUND: Following tilt-induced syncope, blood pressure usually recovers rapidly after tilt back to the horizontal position. However, in some patients, hemodynamic recovery is delayed, a condition recently termed "prolonged post-faint hypotension" (PPFH). The mechanism is thought to be mediated by increased vagal outflow rather than exaggerated peripheral vasodilatation and sympathetic withdrawal. To date, no muscle sympathetic nerve activity (MSNA) recordings have been reported in this condition, so we aimed to confirm that neither vasodilatation nor MSNA withdrawal was responsible. OBJECTIVES: To retrospectively select patients with satisfactory recordings of continuous BP and MSNA during tilt-induced syncope. To compare hemodynamic and MSNA profiles in patients with PPFH to patients with normal recovery (NR) after tilt-back. METHODS: All patients were studied in Christchurch, New Zealand, between 1998 and 2008 using continuous arterial BP monitoring, and microneurographic recordings of MSNA from the right leg. Only patients with satisfactory BP and MSNA data throughout baseline, head-up tilt and presyncope were selected. Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were derived using Modelflow. After baseline measurements, patients were tilted to the head-up 60° position and given GTN spray if asymptomatic after 20 min. Following the onset of presyncope, patients were tilted slowly back to the horizontal. PPFH was defined as systolic BP <85 mmHg for at least 2 min after tilt-back. Measurements were averaged at baseline, early tilt, presyncope, early and late recovery. Within-group comparisons were made between baseline and all other time points. Between-group comparisons were made over all time points. RESULTS: Patients with PPFH (7 males, age 46 ± 5 years, n = 8) and with NR (8 males, age 47 ± 6 years, n = 8) were selected. Presyncope was provoked by GTN in 4/8 patients in each group. In both groups, MAP remained below baseline during early and late recovery: PPFH 84 ± 5 versus 51 ± 5 and 64 ± 5 mmHg (p = 0.001, p = 0.001); NR 104 ± 5 versus 83 ± 5 and 93 ± 5 mmHg (p = 0.001, p = 0.03). However, MAP and HR were lower in the PPFH group (p = 0.004, p = 0.023). During early recovery, CO remained below baseline only in the PPFH group (p = 0.001), whereas TPR remained constant in both groups. In both groups, all MSNA indices tended to remain above baseline levels during early and late recovery. PPFH 25 ± 2 increased to 31 ± 6 and 29 ± 4 bursts/min (p = 0.09, 0.02); NR 23 ± 3 increased to 33 ± 3 and 34 ± 3 bursts/min (p = 0.06, 0.01). CONCLUSIONS: PPFH does not appear to be mediated by exaggerated vasodilatation or sympathetic withdrawal. Delayed recovery of cardiac output by increased vagal outflow is a more likely mechanism.

Prolonged post-faint hypotension can be reversed by dynamic tension.

A severe variant of vasovagal syncope, observed during tilt tests and blood donation has recently been termed "prolonged post-faint hypotension" (PPFH). A 49-year-old male with a life-long history of severe fainting attacks underwent head-up tilt for 20 min, and developed syncope 2 min after nitroglycerine spray. He was unconscious for 40 s and asystolic for 22 s. For the first 2 min of recovery, BP and HR remained low (65/45 mmHg and 40 beats/min) despite passive leg-raising. Blood pressure (and symptoms) only improved following active bilateral leg flexion and extension ("dynamic tension"). During PPFH, when vagal activity is extreme, patients may require central stimulation as well as correction of venous return.

Sleep syncope: important clinical associations with phobia and vagotonia.

OBJECTIVES: To compare demographic and clinical data from patients with sleep syncope to those of patients with "classical" vasovagal syncope [VVS] collected over the last 8 years. DESIGN: Retrospective case-controlled study. SETTING: Syncope unit. PATIENTS AND METHODS: Fifty-four patients with a history suggestive of one or more episodes of sleep syncope (group SS) were matched for age and gender to 108 patients with VVS (control group). A syncope questionnaire was completed immediately before tilt-testing and included frequency, age-of-onset and severity of episodes; situations, postures and perceived triggers; lifetime prevalence of specific phobias; and symptoms during syncope. RESULTS: Group SS were mainly women (65%), mean age of 46±2.1 years, with a mean lifetime total of 5.4±0.83 episodes of sleep syncope. Compared to controls, SS episodes were more likely to start in childhood, 26.9% versus 50% (p=0.005), and more severe, score 2.40±0.11 versus 2.81±0.15 (p=0.03). In group SS: syncope onset whilst lying down was more frequent, 4.6% versus 32.7% (p=0.001); the lifelong prevalence of any specific phobia was higher, 32.4% versus 74.5% (p=0.001), in particular blood injection injury (BII) phobia, 19.4% versus 57.4% (p=0.001); and during attacks, distressing vagal symptoms were more frequent, e.g., abdominal discomfort, 13.9% versus 72.2% (p=0.001). CONCLUSION: Sleep syncope is not rare and is characterised by lifelong, intermittent but severe episodes of vasovagal syncope which may occur in the horizontal position, with distressing abdominal symptoms. BII phobia is strongly associated and may be a predisposing factor or a co-existent disorder in these patients.

Transient loss of consciousness through the eyes of a witness.

OBJECTIVE: To assess the accuracy of eyewitness observations of transient loss of consciousness. METHODS: Two sequential cohorts of psychology students unexpectedly viewed videos of a generalized tonic-clonic seizure (n = 125) and of reflex syncope (n = 104) during a lecture on an unrelated subject. Directly afterward, the students filled in a multiple-choice questionnaire regarding muscle tone, twitches, head deviation, eye closure, gaze deviation, drooling, and facial color. The consensus of experienced neurologists served as a gold standard. Even though not all items could be ascertained from the videos, the full range of questions was included to simulate clinical practice. RESULTS: Of all responses to the observable items on the syncope video (flaccid limbs, twitches of one shoulder, head deviation), 44% were correct, 28% erroneous, and 29% had "I do not know" responses. The observable items on the epilepsy video (stiff limbs, twitches of all limbs, normal facial color, drooling, no head deviation) yielded 60% correct responses, 18% erroneous responses, and 22% "I do not know" responses. Regarding features that were not visible on the videos, 77% of the responses were accurate ("I do not know"), whereas 23% erroneously provided an observation. Of all items observable on both videos, muscle tone was the most accurately recalled item. CONCLUSIONS: An eyewitness account of a single episode of transient loss of consciousness (TLOC) should be interpreted with caution because salient features are frequently overlooked or inaccurately recalled. However, the accuracy of the eyewitness observations of TLOC differs per item; muscle tone was reported with high accuracy.

Analysis of rhythm variation during spontaneous cardioinhibitory neurally-mediated syncope. Implications for RDR pacing optimization: an ISSUE 2 substudy.

BACKGROUND: Little is known of the variations of the heart rate during spontaneous cardioinhibitory neurally-mediated syncope. Their knowledge has both academic and practical implications for the optimization of rate drop response (RDR) pacing mode. METHODS AND RESULTS: We describe variations of the rhythm occurring during 48 syncopal episodes documented by implantable loop recorder. The presyncopal phase of 18 s (interquartile range 9-65) was characterized by a fall in heart rate from 83 +/- 20 bpm to maximal bradycardia or (multiple) asystolic pauses which lasted a median of 19 s (10-30). The recovery phase lasted 22 s (7-52). The total duration of the cardioinhibitory reflex was 85 s (47-116). We then calculated the potential increase in benefit that an optimally programmed drop rate detection could provide compared with a reference Lower Rate detection. Compared with Lower Rate detection (defined as two consecutive beats at 40 bpm), drop rate detection (assumed to be drop size = 20 bpm, detection window = 1 min, and drop rate = 50 bpm) would have been able to introduce intervention pacing, a median of 5.7 s (interquartile range -5.1- -10.4) earlier in 28 cases (58%). CONCLUSION: Cardioinhibitory neurally-mediated reflex varies widely from a few seconds to some minutes. In our data the total duration was <2 min. Optimal RDR programming, being potentially able to anticipate the detection of the cardioinhibitory reflex by a few seconds, could provide an increase in benefit for cardiac pacing therapy in prevention of syncope.

[Terms in use for transient loss of consciousness in the emergency ward; an inventory]. / Gebruikte termen voor 'voorbijgaande bewusteloosheid' op de Eerste Hulp; een inventarisatie.

OBJECTIVE: To investigate the terminology for transient loss of consciousness in use in a Dutch emergency ward and to compare it with European definitions. DESIGN: Descriptive. METHOD: The records of all consecutive patients seen during an eight-week period in the Emergency Clinic of Leiden University Medical Centre, the Netherlands, were reviewed. Patients were enrolled in one of the following Dutch terms was encountered, expressing either a specific form or a general description of non-traumatic transient loss of consciousness (TLOC): 'collaps' (collapse), 'syncope' (syncope), 'flauwvallen' (fainting), 'wegraking' (TLOC) and 'insult' (seizure). The use of these terms was compared with the definitions of the European Society of Cardiology (ESC). RESULTS: The prevalence of a non-traumatic TLOC diagnosis in the Emergency Clinic was 2.9% (123/4300). 'Collaps' was the most frequently used term (53%), followed by 'insult' (31%), 'wegraking' (11%), 'flauwvallen' (3%) and 'syncope' (2%). The term 'collaps' was found to have been used in the context of the ESC category 'syncope' (n=47), TLOC (n=5), 'no TLOC' (n=9) or for situations that could not be classified (n=4). The term 'insult' was used exclusively in the context of epilepsy and the term 'syncope' exclusively in the context of the ESC category 'syncope'. The term 'wegraking' proved to have been used in the context of the ESC category 'TLOC' (n=11), 'epilepsy' (n=1) or for situations that could not be classified (n=1). 'Flauwvallen' was used in the context of the ESC category 'syncope' (n=3) or the category 'no TLOC' (n=1). CONCLUSION: It would be advisable to give the terms mentioned above a specific meaning: reserve 'collaps' for a fall without an obvious external cause, 'wegraking' for transient loss of consciousness without a clear cause, and 'syncope' for loss of consciousness due to temporary low cerebral blood flow.

Diagnostic value of history taking in reflex syncope.

The medical history, in combination with the physical examination and a 12-lead electrocardiogram, plays a key role in the diagnosis and risk stratification of patients with syncope. However, diagnostic clinical criteria are not uniformly applied. In older studies, the diagnostic criteria for vasovagal or reflex syncope often included typical precipitating events and warning symptoms. More recent studies have documented that a variety of unrecognized stressors can trigger reflex syncope and that warning signs and symptoms may be minimal. A characteristic medical history (a trigger and/or prodromi) is enough to diagnose reflex syncope if the risk for a cardiac cause of syncope is low (e. g. patients < 65 yrs, without a history of heart disease and no ECG abnormalities). In elderly subjects with a higher risk of cardiac syncope, the yield of the medical history is lower. However, a prospective study of the value of the medical history for the diagnosis of syncope with long-term follow-up has not been performed.

Epidemiology of reflex syncope.

Cost-effective diagnostic approaches to reflex syncope require knowledge of its frequency and causes in different age groups. For this purpose we reviewed the available literature dealing with the epidemiology of reflex syncope. The incidence pattern of reflex syncope in the general population and general practice is bimodal with peaks in teenagers and in the elderly. In the young almost all cases of transient loss of consciousness are due to reflex syncope. The life-time cumulative incidence in young females ( congruent with 50 %) is about twice as high as in males ( congruent with 25 %). In the elderly, cardiac causes, orthostatic and postprandial hypotension, and the effects of medications are common, whereas typical vasovagal syncope is less frequent. In emergency departments, cardiac causes and orthostatic hypotension are more frequent especially in elderly subjects. Reflex syncope, however, remains the most common cause of syncope, but all-cause mortality in subjects with reflex syncope is not higher than in the general population. This knowledge about the epidemiology of reflex syncope can serve as a benchmark to develop cost-effective diagnostic approaches.

Baroreflex failure: a neglected type of secondary hypertension.

The arterial baroreflex buffers abrupt transients of blood pressure and prevents pressure from rising or falling excessively. In experimental animals, baroreceptor denervation results in temporary or permanent increases in blood pressure level and variability, depending on the extent of denervation. In humans, the clinical syndrome of baroreflex failure may arise from denervation of carotid baroreceptors following carotid body tumour resection, carotid artery surgery, neck irradiation and neck trauma. The syndrome is characterised by acute malignant hypertension and tachycardia followed by labile hypertension and hypotension. Baroreflex failure can be a cause of hypertension and should also be considered in the differential diagnosis of pheochromocytoma. Patients with suspected baroreflex failure should be referred to specialised centres for diagnostic testing and treatment.

A patient with recurrent syncope and ST-elevation on the electrocardiogram.

A 56-year old woman had over 100 episodes of syncope since the age of 8. Because the patient's description of the episodes suggested vasovagal syncope she was studied by a head up tilt test (HUT). Seconds after the uncomplicated HUT the patient experienced a typical syncope with bradycardia, marked ST-elevation and chest pain. After treatment with nifedipine she has had one syncopal spell in a follow up period of 31 months. We conclude that the syncopal events in this patient were caused by a combination of vasovagal syncope and coronary spasm.

Vasovagal syncope interrupting sleep?

Clinical data are reported for 13 patients who were referred with recurrent loss of consciousness at night interrupting their sleep. Most of the patients were women (10 of 13) with a mean age of 45 years (range 21-72 years). The histories were more consistent with vasovagal syncope than with epilepsy. This was supported by electroencephalographic and tilt test results. More polysomnographic monitoring data are required to confirm the diagnosis of vasovagal syncope interrupting sleep. This will be difficult because, although the condition may not be rare, the episodes are usually sporadic.