title: Blood pressure variability and baroreflex sensitivity of a healthy male during cold pressor test that induced development of neurocardiogenic syncope.
abstract: BACKGROUND
  The cold pressor test (CPT) is a recognized physiological technique to evaluate autonomic cardiovascular function. The present case study assessed the cardiovascular response of a healthy adult male during 3 min of CPT.
  
  
  METHODS
  Heart rate (HR) by single-lead electrocardiography and blood pressure (BP) by an arterial tonometer of the participant on a beat-to-beat basis were recorded before and during CPT.
  
  
  RESULTS
  HR during CPT showed a biphasic pattern with an initial increase from baseline (86 bpm) to the first 30 s of CPT (93 bpm) followed by a decrease. It dropped to 51 bpm during the last 30 s of CPT. Systolic blood pressure (SBP) increased from baseline (110 mmHg) to 1 min (122 mmHg) followed by a decrease. SBP immediately after CPT reduced to 57 mmHg. Diastolic blood pressure (DBP) from baseline (71 mmHg) slightly increased to 75 mmHg up to 90 s of the test, thereafter it registered a fall, and during the last 30 s of CPT, DBP fell to 30 mmHg. Stroke volume increased from baseline (75 mL/min) to the first 30 s (99 mL/min), followed by a slight reduction which was maintained till last of the test (70 mL/min). Cardiac output after an initial increase from baseline (6.4 L/min) to the first 30 s (9.2 L/min) decreased to 4.1 L/min during the last 30 s of the test. Baroreflex sensitivity (BRS) from baseline (9.32 ms/mmHg) plummeted to 6.67 ms/mmHg during the first 30 s of CPT followed by an increase, and after CPT, BRS was increased to 15.23 ms/mmHg. Other cardiovascular parameters such as myocardial contractility (dp/dt), total peripheral resistance, and mean arterial pressure were reduced in the individual at the time of loss of consciousness that occurred at the end of the last 30 s of CPT.
  
  
  CONCLUSIONS
  The present case study described the modulation of cardiovascular functions of a healthy male during CPT, which finally led to the development of neurocardiogenic syncope characterized by hypotension and bradycardia.
authors.forename: Biswajit
authors.identifier: http://orcid.org/0000-0002-0783-1400
authors.initials: B
authors.lastname: Sinha
authors.forename: Dinesh K
authors.initials: DK
authors.lastname: Dubey
mesh_terms: D000328:Adult; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology*; D002319:Cardiovascular System / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D007022:Hypotension / Q000503:physiopathology; D008297:Male; D013318:Stroke Volume / Q000502:physiology