Novel Methods for Quantification of Vasodepression and Cardioinhibition During Tilt-Induced Vasovagal Syncope

Abstract

Rationale: Assessing the relative contributions of cardioinhibition and vasodepression to the blood pressure (BP) decrease in tilt-induced vasovagal syncope (T-VVS) requires methods that reflect BP physiology accurately. Objective: To assess the relative contributions of cardioinhibition and vasodepression to T-VVS using novel methods. Methods and Results: We studied the parameters determining BP, i.e. stroke volume (SV), heart rate (HR) and total peripheral resistance (TPR), in 163 patients with T-VVS documented by continuous ECG and video EEG monitoring. We defined the beginning of cardioinhibition as the start of a heart rate decrease (HR) before syncope, and used logarithms of SV-, HR- and TPR-ratios to quantify the multiplicative relation BP=SV·HR·TPR. We defined three stages before syncope and two after it based on direction changes of these parameters. The earliest BP decrease occurred nine minutes before syncope. Cardioinhibition was observed in 91% of patients at a median time of 58 s. before syncope. At that time SV had a strong negative effect on BP, TPR a lesser negative effect, while HR had increased (all p<0.001). At the onset of cardioinhibition, median HR was at 98 bpm higher than baseline. Cardioinhibition thus initially only represented a reduction of the corrective HR increase, but was nonetheless accompanied by an immediate acceleration of the ongoing BP decrease. At syncope, SV and HR contributed similarly to the BP decrease (p<0.001), while TPR did not affect BP. Conclusions: The novel methods allowed the relative effects of SV, HR and TPR on BP to be assessed separately, even though all act together. The two major factors lowering BP in T-VVS were reduced SV and cardioinhibition. We suggest that the term 'vasodepression' in reflex syncope should not be limited to reduced arterial vasoconstriction, reflected in TPR, but should also encompass venous pooling, reflected in SV.

Cardiac pacing in severe recurrent reflex syncope and tilt-induced asystole

“… 15–18 In brief, since at the time of impending syncope stroke volume and heart rate contribute similarly to blood pressure, an early heart rate increase driven by CLS may partly prevent blood pressure fall due to the vasodepressor reflex. 19 …”

Recommendations for tilt table testing and other provocative cardiovascular autonomic tests in conditions that may cause transient loss of consciousness : Consensus statement of the European Federation of Autonomic Societies (EFAS) endorsed by the American Autonomic Society (AAS) and the European Academy of Neurology (EAN)

“…Several commercial devices are available for non-invasive beat-to-beat measurements of blood pressure and heart rate using finger photoplethysmography and the volume clamp method (Imholz et al, 1998). Additional software yields estimates of other circulatory parameters including stroke volume, cardiac output and total peripheral resistance; these may be used to quantify the relative contributions of vasodilation and cardioinhibition (van Dijk et al, 2020), but this is not required for routine clinical testing.…”

Tilt testing remains a valuable asset

“… 43 Recent studies of TT methodology have provided greater insight into the sequence of haemodynamic events during VVS and may permit more appropriate application of pacing systems. 39 , 44 , 45 The impact of reducing venous return and stroke volume during evolving VVS seems to be key to understanding the utility and limitations of pacing intervention. 44 …”

“… 39 , 44 , 45 The impact of reducing venous return and stroke volume during evolving VVS seems to be key to understanding the utility and limitations of pacing intervention. 44 …”