Evaluation of cold face test bradycardia by means of spectral analysis

Abstract

The cold face test (CFT) is a non-invasive challenge maneuver of the autonomic nervous system which activates the peripheral sympathetic and the cardiac parasympathetic nervous system and induces peripheral vasoconstriction and bradycardia. The physiology of CFT-induced bradycardia is still controversial. The heart rate decrease might result from a direct central up-regulation of cardiovagal activity or might be a secondary effect of baroreceptor activation or of changes of respiration. The purpose of this study was to analyze the origin of CFT-induced bradycardia. To evaluate the influence of respiration on bradycardia during CFT, we studied cardiac responses in 10 healthy volunteers during CFT (0-1 degrees C cold compresses for 60 s) with three different respiratory patterns: one with spontaneous and two with paced respiration (6 and 15 cycles/minute). We continuously monitored heart rate (HR), blood pressure (BP) and respiration and determined heart rate variability by assessment of coefficient of variation (CV), standard deviation (SD) and the root mean square of successive differences (RMSSD) of HR as well as low (LF) and high (HF) frequency spectra power of HR and BP. When coherence was above 0.5, we calculated the transfer function gain between HR and respiration in the HF band, as an index of respiratory sinus arrhythmia, and between HR and BP in the LF band, as an index of baroreflex sensitivity. HR decreased and BP increased significantly during the three types of CFT. The decrease of HR and the increase of BP, of time and frequency domain parameters did not differ between the three breathing patterns. Respiration, and HF and LF power of respiration did not change during CFT. The gain of the HF-transfer function between HR and respiration and the LF-transfer function gain between HR and BP increased significantly during CFT, but the increase did not differ between the three breathing patterns. The increase of the gain of both transfer functions is most likely due to an increase of vagal traffic and together with the unchanged respiratory pattern suggests that CFT-induced bradycardia is not due to baroreflex or respiratory influences, but seems to result from central vagal activation.

Sustained increases in blood pressure elicited by prolonged face cooling in humans

“…It is well established that face cooling elicits a pressor response in humans for up to 180 s (1,3,7,11,14,15,18,19,21,22). Data from the present study extend these findings and show that face cooling-induced increases in blood pressure can be sustained for at least 15 min (Fig.…”

“…Cooling of the forehead and cheeks evokes a similar, yet less pronounced, response in humans (1,3,7,11,14,15,18,19,21,22), which occurs secondary to stimulation of the cold afferents of the trigeminal nerve (10,17). Face cooling in humans simultaneously stimulates the parasympathetic and sympathetic nervous systems, evoking bradycardia and peripheral vasoconstriction (1,3,7,11,14,15,18,19,21,22). In humans, reductions in heart rate are not sufficient to reduce cardiac output (3).…”

“…In humans, reductions in heart rate are not sufficient to reduce cardiac output (3). Therefore, blood pressure increases as a result of systemic peripheral vasoconstriction (1,3,7,11,14,15,18,19,21,22).…”

“…The hemodynamic responses to face cooling in humans have only been studied up to 180 s in duration (1,3,7,11,14,15,18,19,21,22). Thus, it is unknown whether the relative hypertensive responses elicited by face cooling, in addition to the temporal dynamics of parasympathetic and sympathetic activation, are sustained beyond 180 s. The diving reflex in diving mammals and birds persists for the duration of the dive (4).…”

Effect of ice water ingestion on cardiac autonomic reactivity in healthy subjects

“…[1] Human studies have shown vagal attenuation in response to immersion of face and hand in ice water. [2][3][4] Literatures have investigated whether water drinking in normal subjects affected peripheral sympathetic neural discharge and its effect on vascular resistance. The last two decades have witnessed the recognition of a significant relationship between the autonomic nervous system and cardiovascular mortality, including sudden cardiac death.…”