The cold face test: A non-baroreflex mediated test of cardiac vagal function

Ramesh K. Khurana, Roger Wu

Research output: Contribution to journalArticlepeer-review

39 Scopus citations

Abstract

Application of cold to the face evokes potent bradycardia and a pressor response, similar to the diving reflex. However, the role of the baroreceptors in this response is unclear. Ten healthy controls and two patients with baroreflex impairment were recruited. A cold face test (CFT) was induced by the application of three cold packs (0.5°C) to the face. Heart rate (ECG), blood pressure (Finapres) and skin temperature (forehead electrode) were recorded continuously. All data were analyzed using unpaired Students t-tests, and expressed as mean ± SD. In all controls, CFT induced bradycardia. The mean onset latency was 5.6 ± 4.6 s, and the maximal bradycardia was seen at 35.8 ± 15.8 s. Systolic blood pressure increased in eight controls, with a mean onset latency of 18.8 ± 16.6 s and a peak rise at 38.7 ± 22.7 s. In the controls, bradycardia preceded the pressor response. The heart rate and blood pressure changes during CFT had a longer latency than baroreflex evoked responses. Moreover, one subject had bradycardia despite a fall in blood pressure. The two patients had abnormal Valsalva ratios and no change in heart rate during tilt, indicating impairment of the baroreflex. However, both their heart rate and blood pressure responses to CFT were normal. These data are further evidence of the limited role of the baroreflex in the autonomic responses to CFT. They suggest that the CFT may be of use in assessing the integrity of the efferent cardiovascular autonomic pathways in patients with suspected baroreflex impairment.

Original languageEnglish (US)
Pages (from-to)202-207
Number of pages6
JournalClinical Autonomic Research
Volume16
Issue number3
DOIs
StatePublished - Jun 2006
Externally publishedYes

Keywords

  • Autonomic control
  • Baroreflex
  • Bradycardia
  • Cold face test
  • Diving response

ASJC Scopus subject areas

  • Endocrine and Autonomic Systems
  • Clinical Neurology

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