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.
The simple faint is secondary to hypotension and bradycardia resulting in transient loss of consciousness. According to Ohm's law applied to the circulation, BP = SVR × CO, hypotension can result ...from a decrease in systemic vascular resistance (SVR), cardiac output (CO), or both. It is important to understand that when blood pressure (BP) is falling, SVR and CO do not change reciprocally as they do in the steady state. In 1932, Lewis, assuming that decreased SVR alone accounted for hypotension, defined "the vasovagal response" along pathophysiologic lines to denote the association of vasodilation with vagal-induced bradycardia in simple faint. Studies performed by Barcroft and Sharpey-Schafer between 1940 and 1950 used volume-based plethysmography to demonstrate major forearm vasodilation during extreme hypotension and concluded that the main mechanism for hypotension was vasodilation. Plethysmographic measurements were intermittent and not frequent enough to capture rapid changes in blood flow during progressive hypotension. However, later investigations by Weissler, Murray, and Stevens performed between 1950 and 1970 used invasive beat-to-beat BP measurements and more frequent measurements of CO using the Fick principle. They demonstrated that CO significantly fell before syncope, and little vasodilation occurred until very late in the vasovagal reaction Thus, since the 1970s, decreasing cardiac output rather than vasodilation has been regarded as the principal mechanism for the hypotension of vasovagal syncope.
Syncope is defined as transient loss of consciousness as a result of cerebral hypoperfusion. Electroencephalography during syncope shows either a 'slow-flat-slow' or a 'slow' pattern. The first is ...believed to denote more severe hypoperfusion. Although the diagnosis of vasovagal syncope relies primarily on history taking, there is limited evidence regarding the relative importance of various clinical features, and none that relate them to the severity of electroencephalographic changes. The aim of this investigation was to study symptoms, signs and electroencephalographic changes with a 1 s resolution using electroencephalography and video data in 69 cases of tilt-induced vasovagal syncope. The main finding was that flattening of the electroencephalograph indicated more profound circulatory changes: the 'slow-flat-slow' group had a lower minimum blood pressure, longer maximum RR-interval, contained more cases with asystole and had a longer duration of loss of consciousness than the 'slow' group. Second, we describe a range of signs, including some that have rarely been reported in syncope, e.g. oral automatisms. Third, signs occurred at different rates depending on electroencephalographic flattening, suggesting a classification of syncopal signs. Type A signs (e.g. loss of consciousness, eye opening and general stiffening) develop during the first slow phase, stay present during flattening and stop in the second slow phase. Type B (particularly myoclonic jerks) occur when the electroencephalograph is slow but not flat: their abolition with electroencephalographic flattening suggests dependence on cortical activity. Type C signs (making sounds, roving eye movements and stertorous breathing) occur only in the flat phase, whereas type D (dropping the jaw and snoring) may occur either in slow or flat phases. In conclusion, our findings provide a detailed assessment of clinical symptoms in relation to electroencephalographic (EEG) changes during tilt-induced syncope.
Abstract Background Although orthostatic hypotension (OH) is recognized as one of the main non-motor symptoms of Parkinson’s disease (PD), there is inconsistent evidence about the prevalence of OH in ...PD. To estimate the prevalence of OH in PD more precisely we conducted a systematic review of the literature. Methods From PubMed and Embase searches with predefined inclusion criteria, we identified studies published up till December 2009. Prevalence numbers from studies were pooled using a non-linear random-effects meta-analysis. Results We found 25 studies from which the prevalence of OH could be calculated. The pooled estimate of the point prevalence of OH in PD was 30·1% (95% CI: 22·9% to 38·4%). We found a large statistical heterogeneity between studies which could not be reduced by several subgroup analyses. Conclusions The estimated prevalence of OH in PD is 30%. However, due to the large heterogeneity between studies this pooled estimate should be interpreted with caution. More data from unselected population-based cohorts are needed.
Sleep syncope: a prospective cohort study Jardine, David L.; Davis, Jonathan; Frampton, Christopher M. ...
Clinical autonomic research,
02/2022, Letnik:
32, Številka:
1
Journal Article
Recenzirano
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.
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