Hemodynamic Patterns and Spectral Analysis of Heart Rate Variability during Dialysis Hypotension

Intradialytic hypotension, a major source of morbidity during hemodialysis and ultrafiltration, is often accompanied by paradoxical bradycardia. Relatively little is known about the sequential changes in autonomic nervous system activity up to and during the hypotensive episode. Continuous, beat-to-beat measurements of BP and heart rate were made during hemodialysis in patients prone (n = 8) and not prone (n = 11) to develop intradialytic hypotension. Off-line spectral analysis of heart rate variability (HRV) was performed to assess changes in autonomic nervous system activity during dialysis sessions both with and without hypotension. The low frequency (LF) component of HRV is thought to correlate with sympathetic nervous system activity, the high frequency (HF) component with that of the parasympathetic nervous system. In the sessions not complicated by symptomatic hypotension (n = 26), mean arterial BP (MAP) hardly fell, whereas heart rate increased from 77 ± 2 to 89 ± 5 bpm (P < 0.05). The LF component of HRV increased from 45.2 ± 5.0 normalized units (nu) to 59.9 ± 4.9 nu (P < 0.05), whereas the HF component fell from 54.8 ± 5.0 to 40.2 ± 4.4 nu (P < 0.05). These changes agree with compensatory baroreflex-mediated activation of the sympathetic nervous system (and suppressed parasympathetic activity) during ultrafiltration-induced intravascular volume depletion. In the sessions complicated by severe symptomatic hypotension (n = 22), the changes in heart rate and the results of spectral analysis of HRV were similar to those reported above up to the moment of sudden symptomatic (nausea, vomiting, dizziness, cramps) hypotension, whereas MAP had already fallen gradually from 94 ± 3 to 85 ± 3 mmHg (P < 0.05). The sudden further reduction in MAP (to 55 ± 2 mmHg, P < 0.02) was invariably accompanied by bradycardia (heart rate directly before hypotension 90 ± 2 bpm, during hypotension 69 ± 3 bpm, P < 0.002). The LF component of HRV fell from 62.8 ± 4.6 nu directly before to 40.0 ± 3.7 nu (P < 0.05) during hypotension, whereas the HF component increased from 37.9 ± 4.7 to 60.3 ± 3.7 nu (P < 0.05). These findings agree with activation of the cardiodepressor reflex, involving decreased sympathetic and increased parasympathetic nervous system activity, respectively. These findings indicate that activation of the sympatho-inhibitory cardiodepressor reflex (Bezold-Jarisch reflex), which is a physiologic response to a critical reduction in intravascular volume and cardiac filling, is the cause of sudden intradialytic hypotension.