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ESRD Patients Have Altered Pattern of Heart Rate Variability Responses to Graded Lower Body Negative Pressure
Author(s) -
Ye Kara,
Downey Ryan,
Liao Peizhou,
Park Jeanie
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.863.1
Subject(s) - medicine , hypovolemia , orthostatic vital signs , heart rate variability , heart rate , cardiology , blood pressure , autonomic nervous system , orthostatic intolerance , baroreflex , hemodynamics , anesthesia
End stage renal disease (ESRD) patients have autonomic neuropathy that contributes to increased cardiovascular (CV) risk. The normal autonomic response to orthostatic stress induced by hypovolemia is to increase sympathetic nervous system (SNS) and decrease parasympathetic nervous system (PNS) activation in order to maintain arterial blood pressure. Prior studies have shown that healthy individuals have decreases in heart rate variability (HRV) in response to increased orthostatic stress induced by graded lower body negative pressure (LBNP), reflective of increased SNS and decreased PNS activation to the heart in response to central hypovolemia. The objective of this study was to determine if ESRD patients have intact HRV responses during orthostatic stress. Given that ESRD patients have autonomic neuropathy, we hypothesized that ESRD patients have lower HRV at baseline, and an inability to adjust SNS and PNS activity to the heart in response to orthostatic stress. We measured continuous beat‐to‐beat blood pressure and ECG at baseline for 10 minutes, and during orthostatic stress induced via increasing doses of LBNP (−5, −10, −15, −20, −30, and −40 mmHg) applied for 3 minutes at each dose in ESRD patients and healthy controls. HRV was quantified as: 1)the standard deviation of the normal R‐R interval (SDNN), which is reflective of total autonomic activity; 2) the root mean square of the successive differences between adjacent N‐N intervals (RMSSD), and 3) percentage of adjacent NN intervals that differ by greater than 50 msec (pNN50), which are primarily reflective of PNS activity to the heart. We observed that baseline SDNN ( p =0.001), RMSSD ( p =0.004), and pNN50 ( p =0.016) were significantly lower in ESRD patients compared to healthy controls, suggestive of chronically high SNS and low PNS activity in ESRD patients. The slopes of change in RMSSD and pNN50 with increasing LBNP were significantly different between ESRD and controls ( p =0.004 and p <0.001, respectively). Whereas healthy controls exhibited gradual decreases in RMSSD and pNN50 with increasing LBNP, signifying decreasing PNS activity to the heart during orthostatic stress, ESRD patients exhibited constant and unchanging RMSSD and pNN50 values, suggesting failure to adjust PNS activity to the heart during orthostatic stress. In conclusion, ESRD patients had low baseline HRV measurements, indicative of high SNS and low PNS activity that could contribute to cardiovascular complications in this population. Unlike controls, ESRD patients did not demonstrate a withdrawal of PNS activation to the heart during orthostatic stress. Failure to adjust autonomic responses during orthostatic stress in ESRD may contribute to orthostatic intolerance and increased CV risk in this patient population. Support or Funding Information Supported by NIH HL‐098744, NIH DK‐101390, VA Merit I01CX001065, and Satellite Healthcare, a not‐for‐profit renal care provider.