The Cardiorespiratory Coupling as a Background for Blood Pressure Decrease

Abstract

The role of cardiorespiratory coupling cannot be overemphasized. Cardiorespiratory coupling has many potential benefits in maintaining homeostasis. One of manifestation of cardiorespiratory coupling is respiratory sinus arrhythmia observed at respiratory rate 6 breaths/ minute. Multiple factors, including mechanical coupling, are responsible for the fluctuation of HR and BP. However, the fine mechanisms of the autonomic, cardiovascular, and respiratory interactions till now remains unclear.A total of 156 international students were recruited from the V.N. Karazin Kharkiv National University. The sitting position was taken as a baseline according to requirements of the spirometry system. The ECG was continuously recorded at the rest and during slow breathing at 6 breaths/minute. The respiratory rate (RR) and tidal volume (TV) were recorded at the end of each stage for one minute using SPIROCOM pc based systems (XAI‐Medica, Ukraine). Systolic and diastolic blood pressure (SBP and DBP) were recorded by means automatic digital sphygmomanometer (OMRON EVOLV, Japan). The low and high frequency heart rate variability (LF and HF HRV) power were computed with CardioLab CS by fast Fourier transforming. The repeated measures MANOVA with Bonferroni correction (SPSS 22) was used to test for effects of slow breathing on HR, SBP, DBP, LnLF, LnHF, tidal volume (TV), minute ventilation (MV), and RR variables. Predictors of HR, SBP, DBP, TV, MV., and RR to slow breathing were determined using stepwise multiple linear regression analysis. Written informed consent was obtained from each participant.In the current study the slowing respiratory rate to 6 breaths/min increased HR (P<0.001) (not shown), decreased SBP (P<0.001), decreased DBP (P=0.003), increased LnLF (P<0001), increased TV (P<0.001), and decreased RR (not shown, Р<0.001). The stepwise multiple linear regression analysis revealed that at rest HR and RR were negatively associated with LnHF power (Table 1, P<0.001 for both), while at slow breathing stage the HR was negatively associated with both LnHF and LnLF power (Table 2, P<0.001 and P=0.004, respectively). If the HF power is widely used as an index of cardiovagal activity, interpretation of the LF power is more controversal. We proceeded from our hypothesis that LF HRV power is a measure of baroreflex‐mediated sympathoinhibition. At rest both SBP and DBP were positively associated with LnLF by LnHF interaction, while at slow breathing stage they were negatively associated only with LnLF power. The resting TV and MV were positively associated with LnLF power, also, the MV with LnHF by height and BMI interaction. But at slow breathing stage only the height and BMI were independent variables remaining in these models (Table 2, Models 4 and 5).Taken together, these findings indicate that the same autonomic variables control respiratory function in parallel with cardiovascular system.