Clinical Autonomic Research | 2021

Observations of a syncope doctor during self-induced (near)syncope episodes

 

Abstract


This contribution to the special issue to commemorate the 30th anniversary of Clinical Autonomic Research summarizes my observations as a clinician and clinical physiologist on the hemodynamic responses and accompanying symptoms of self-induced (near)syncope elicited by three different provocations: (1) vasovagal near-syncope; (2) fainting lark; and, (3) sinus arrest. In the early 1990s, Roger Hainsworth introduced tilt-table testing combined with the application of lower body negative pressure (LBNP) using a vacuum cleaner. The provocation caused a large shift of blood from the thorax to the lower body providing a progressive test of orthostatic tolerance [2]. In 1995 the Amsterdam Medical Center syncope unit obtained a tilt-table-LBNP device for physiological studies. Because of my interest in the temporal course of the hemodynamic changes during a vasovagal presyncope, I induced an episode onto myself under the supervision of two experienced syncope doctors (Fig. 1a) [3]. At 38–40 min, increasing LBNP to a negative pressure of − 40 mmHg induced a classical vasovagal reaction with decreases in heart rate (HR), cardiac output, and BP (Fig. 1b). My lowest BP was 30/20 mmHg. I experienced a feeling of warmth followed by lightheadedness but did not faint. After a rapid tilt-down and the discontinuation of the LBNP, there was a recovery of my BP to baseline levels followed by an overshoot with almost immediate disappearance of my lightheadedness. I did not experience visual disturbances. The classical fainting lark involves squatting in a full knee bend position and hyperventilating by taking about 20 deep breaths. The subject then stands up suddenly and performs a forced expiration against a closed glottis (i.e., a Valsalva maneuver). The fainting lark combines the effects of systemic arterial hypotension induced by acute vasodilatation of the lower limbs (the combination of standing up and the post-ischemic effect of squatting) and decreased cardiac output (effects of arising and raised intrathoracic pressure) and cerebral vasoconstriction induced by hypocapnia (due to hyperventilation) [9]. Using the fainting lark, I induced syncope in myself because of my interest in the time course of the BP changes and accompanying symptoms during this provocation [8]. No such tracings were available in the literature. The fainting lark was performed with minimal straining in order to prevent deep prolonged hypotension with myoclonic jerks [4]. The experiment was supervised by two experienced syncope doctors. I had a precipitous and deep fall in BP when I performed the maneuver. About 4 s after the onset of the fall in BP I experienced a short-lasting lightheadedness and blacked out. The duration of the loss of consciousness was 2–3 s. My lowest BP was 40/20 mmHg, which, upon lying down, rapidly increased with an overshoot (Fig. 1c). In September 2015 I experienced several episodes of severe lightheadedness when walking in a supermarket. I experienced no other symptoms. I recognized the sensation as identical to those induced by the self-induced syncope episodes described above immediately and presented myself to the cardiac emergency department in the Amsterdam Medical Center. My physical exam was normal. My ECG showed periods of sinus arrest up to 5–8 s and ST elevations compatible with pericarditis (Fig. 1d). In retrospect, I did have mild chest pain that became worse on lying down in the days before the presyncope. Using the ECG monitor in the coronary care unit I made the following observations during admission. In the supine position, periods of asystole up to 7 s did not cause any symptoms. In the upright position, standing against the bed, episodes of 5–7-s asystole elicited severe lightheadedness, but visual disturbances or near-syncope did not occur. The timing of the onset of lightheadedness was very reproducible during about five episodes. I was diagnosed with a sick sinus syndrome and implanted with a dual-chamber pacemaker. A causal relation with the * Wouter Wieling [email protected]

Volume None
Pages 1-3
DOI 10.1007/s10286-021-00769-7
Language English
Journal Clinical Autonomic Research

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