Diagnosis and treatment of orthostatic hypotension.

Orthostatic hypotension is an unusually large decrease in blood pressure on standing that increases the risk of adverse outcomes even when asymptomatic. Improvements in haemodynamic profiling with continuous blood pressure measurements have uncovered four major subtypes: initial orthostatic hypotension, delayed blood pressure recovery, classic orthostatic hypotension, and delayed orthostatic hypotension. Clinical presentations are varied and range from cognitive slowing with hypotensive unawareness or unexplained falls to classic presyncope and syncope. Establishing whether symptoms are due to orthostatic hypotension requires careful history taking, a thorough physical examination, and supine and upright blood pressure measurements. Management and prognosis vary according to the underlying cause, with the main distinction being whether orthostatic hypotension is neurogenic or non-neurogenic. Neurogenic orthostatic hypotension might be the earliest clinical manifestation of Parkinson's disease or related synucleinopathies, and often coincides with supine hypertension. The emerging variety of clinical presentations advocates a stepwise, individualised, and primarily non-pharmacological approach to the management of orthostatic hypotension. Such an approach could include the cessation of blood pressure lowering drugs, adoption of lifestyle measures (eg, counterpressure manoeuvres), and treatment with pharmacological agents in selected cases.

Sleep syncope: a prospective cohort study.

PURPOSE: Sleep syncope is defined as a form of vasovagal syncope which interrupts sleep. Long term follow-up has not been reported. METHODS: Between 1999 and 2013 we diagnosed vasovagal syncope in 1105 patients of whom 69 also had sleep syncope. We compared these 69 patients in the sleep syncope group to 118 patients with classical vasovagal syncope consecutively investigated between 1999 and 2003. We compared baseline demography, syncope history, tilt test results and follow-up findings. RESULTS: At baseline, age and gender distribution (mean ± standard deviation) of the classical VVS and sleep synocope groups were similar: 46 ± 21 vs. 47 ± 15 years (p = 0.53), and 55% versus 66% female (p = 0.28), respectively. Abdominal discomfort and vagotonia were more frequent in sleep syncope patients: 80% versus 8% and 33% versus 2% (p < 0.001). Childhood syncope and blood-needle phobia were also more frequent in sleep syncope patients: 58% versus 15% and 69% versus 19% (p < 0.001). Positive tilt test results were similar for the two groups (93% [classical VVS] vs. 91%; p = 0.56). Blood pressure, heart rate and stroke volume changed in a similar manner from baseline to syncope (p = 0.32, 0.34 and 0.18, respectively). Mean duration of follow-up for the classical VVS and sleep syncope groups, as recorded in the electronic records, were 17 (3-21) and 15 (7-27) years, respectively. Rates of mortality and of permanent pacemaker insertion were similar in the two groups: 16.2% (classical VVS) versus 7.6% (p = 0.09) and 3% (classical VVS) versus 3% (p = 0.9). Incidence of sleep episodes decreased from 1.9 ± 3 to 0.1 ± 0.3 episodes per year (p < 0.001). CONCLUSION: Sleep syncope is a subtype of vasovagal syncope with characteristic symptoms. Despite the severity of the sleep episodes, the prognosis is very good. Very few patients require permanent pacing, and nearly all respond to education and reassurance.

Diagnostic criteria for initial orthostatic hypotension: a narrative review.

Abnormalities in orthostatic blood pressure changes upon active standing are associated with morbidity, mortality, and reduced quality of life. However, over the last decade, several population-based cohort studies have reported a remarkably high prevalence (between 25 and 70%) of initial orthostatic hypotension (IOH) among elderly individuals. This has raised the question as to whether the orthostatic blood pressure patterns in these community-dwelling elderly should truly be considered as pathological. If not, redefining of the systolic cutoff values for IOH (i.e., a value ≥ 40 mmHg in systolic blood pressure in the first 15 s after standing up) might be necessary to differ between normal aging and true pathology. Therefore, in this narrative review, we provide a critical analysis of the current reference values for the changes in systolic BP in the first 60 s after standing up and discuss how these values should be applied to large population studies. We will address factors that influence the magnitude of the systolic blood pressure changes following active standing and the importance of standardization of the stand-up test, which is a prerequisite for quantitative, between-subject comparisons of the postural hemodynamic response.

Systemic and cerebral circulatory adjustment within the first 60 s after active standing: An integrative physiological view.

Transient cardiovascular and cerebrovascular responses within the first minute of active standing provide the means to assess autonomic, cardiovascular and cerebrovascular regulation using a real-world everyday stimulus. Traditionally, these responses have been used to detect autonomic dysfunction, and to identify the hemodynamic correlates of patient symptoms and attributable causes of (pre)syncope and falls. This review addresses the physiology of systemic and cerebrovascular adjustment within the first 60 s after active standing. Mechanical factors induced by standing up cause a temporal mismatch between cardiac output and vascular conductance which leads to an initial blood pressure drops with a nadir around 10 s. The arterial baroreflex counteracts these initial blood pressure drops, but needs 2-3 s to be initiated with a maximal effect occurring at 10 s after standing while, in parallel, cerebral autoregulation buffers these changes within 10 s to maintain adequate cerebral perfusion. Interestingly, both the magnitude of the initial drop and these compensatory mechanisms are thought to be quite well-preserved in healthy aging. It is hoped that the present review serves as a reference for future pathophysiological investigations and epidemiological studies. Further experimental research is needed to unravel the causal mechanisms underlying the emergence of symptoms and relationship with aging and adverse outcomes in variants of orthostatic hypotension.

Diagnostic accuracy of evaluation of suspected syncope in the emergency department: usual practice vs. ESC guidelines.

BACKGROUND: Syncope is a frequent reason for referral to the emergency department. After excluding a potentially life-threatening condition, the second objective is to find the cause of syncope. The objective of this study was to assess the diagnostic accuracy of the treating physician in usual practice and to compare this to the diagnostic accuracy of a standardised evaluation, consisting of thorough history taking and physical examination by a research physician. METHODS: This prospective cohort study included suspected (pre) syncope patients without an identified serious underlying condition who were assessed in the emergency department. Patients were initially seen by the initial treating physician and the usual evaluation was performed. A research physician, blinded to the findings of the initial treating physician, then performed a standardised evaluation according to the ESC syncope guidelines. Diagnostic accuracy (proportion of correct diagnoses) was determined by expert consensus after long-term follow-up. RESULTS: One hundred and one suspected (pre) syncope patients were included (mean age 59 ± 20 years). The usual practice of the initial treating physicians did not in most cases follow ESC syncope guidelines, with orthostatic blood pressure measurements made in only 40% of the patients. Diagnostic accuracy by the initial treating physicians was 65% (95% CI 56-74%), while standardised evaluation resulted in a diagnostic accuracy of 80% (95% CI 71-87%; p = 0.009). No life-threatening causes were missed. CONCLUSIONS: Usual practice of the initial treating physician resulted in a diagnostic accuracy of 65%, while standardised practice, with an emphasis on thorough history taking, increased diagnostic accuracy to 80%. Results suggest that the availability of additional resources does not result in a higher diagnostic accuracy than standardised evaluation, and that history taking is the most important diagnostic test in suspected syncope patients. Netherlands Trial Registration: NTR5651. Registered 29 January 2016, https://www.trialregister.nl/trial/5532.

Pacing in vasovagal syncope: A physiological paradox?

The physiological principles underlying pacemaker treatment in patients with vasovagal syncope have never been reviewed. Current knowledge suggests that pacing the right heart is unlikely to correct blood pressure during a vasovagal reaction. In adults, the reason for this is that stroke volume is dictated by central blood volume contained in the cardiopulmonary vessels within the chest (ie, left ventricular preload). Preceding posture-triggered vasovagal syncope, there is a significant fall in central blood volume and therefore in stroke volume and cardiac output long before the onset of bradycardia. This explains why high rate cardiac pacing does not improve cardiac output or blood pressure during presyncope. Contradictory results between physiological theory and trial evidence underlying pacemaker treatment at present cannot be explained. Placebo effects during pacing for vasovagal syncope should be considered. More work is needed to solve the dilemma.

Hemodynamic Mechanisms Underlying Initial Orthostatic Hypotension, Delayed Recovery and Orthostatic Hypotension.

OBJECTIVES: Continuous noninvasive blood pressure (BP) measurement enables us to observe rapid changes in BP and to study underlying hemodynamic mechanisms. This study aimed to gain insight into the pathophysiological mechanisms underlying short-term orthostatic BP recovery patterns in a real-world clinical setting with (pre)syncope patients. SETTING AND PARTICIPANTS: In a prospective cohort study, the active lying-to-standing test was performed in suspected (pre)syncope patients in the emergency department with continuous noninvasive finger arterial BP measurement. MEASURES: Changes in systolic BP, cardiac output (CO), and systemic vascular resistance (SVR) were studied in normal BP recovery, initial orthostatic hypotension, delayed BP recovery, and sustained orthostatic hypotension. RESULTS: In normal recovery (n = 47), ΔBP at nadir was -24 (23) mmHg, with a CO change of +10 (21%) and SVR of -23 (21%). In initial orthostatic hypotension (n = 7) ΔBP at nadir was -49 (17) mmHg and CO and SVR change was -5 (46%) and -29 (58%), respectively. Delayed recovery (n = 12) differed significantly from normal recovery 30 seconds after standing, with a ΔBP of -32 (19) vs 1 (16) mmHg, respectively. Delayed recovery was associated with a significant difference in SVR changes compared to normal recovery, -17 (26%) vs +4 (20%), respectively. There was no difference in CO changes. In sustained orthostatic hypotension (n = 16), ΔBP at 180 seconds after standing was -39 (21) mmHg, with changes in CO of -16 (31%) and SVR of -9 (20%). CONCLUSIONS/IMPLICATIONS: Hemodynamic patterns following active standing are heterogeneous and differ across orthostatic BP recovery patterns, suggesting that volume status, medication use, and autonomic dysfunction should all be taken into account when evaluating these patients. Moreover, results suggest that a delayed BP recovery is associated with an impaired increase in SVR in a significant proportion of individuals, implying that physicians treating older adults with hypertension should consider the possible negative effect of intensive hypertension treatment on initial orthostatic blood pressure control.

The pathophysiology of the vasovagal response.

In part I of this study, we found that the classical studies on vasovagal syncope, conducted in fit young subjects, overstated vasodilatation as the dominant hypotensive mechanism. Since 1980, blood pressure and cardiac output have been measured continuously using noninvasive methods during tilt, mainly in patients with recurrent syncope, including women and the elderly. This has allowed us to analyze in more detail the complex sequence of hemodynamic changes leading up to syncope in the laboratory. All tilt-sensitive patients appear to progress through 4 phases: (1) early stabilization, (2) circulatory instability, (3) terminal hypotension, and (4) recovery. The physiology responsible for each phase is discussed. Although the order of phases is consistent, the time spent in each phase may vary. In teenagers and young adults, progressive hypotension during phases 2 and 3 can be driven by vasodilatation or falling cardiac output. The fall in cardiac output is secondary to a progressive decrease in stroke volume because blood is pooled in the splanchnic veins. In adults a fall in cardiac output is the dominant hypotensive mechanism because systemic vascular resistance always remains above baseline levels.