Intracardiac origin of heart rate variability, pacemaker funny current and their possible association with critical illness.
2013
Heart rate variability (HRV) is an indirect estimator of autonomic modulation of heart rate and is considered a
risk marker in critical illness, particularly in heart failure and severe sepsis. A reduced HRV has been found in critically ill
patients and has been associated with neuro-autonomic uncoupling or decreased baroreflex sensitivity. However, results
from human and animal experimental studies indicate that intracardiac mechanisms might also be responsible for interbeat
fluctuations. These studies have demonstrated that different membrane channel proteins and especially the so-called
‘funny’ current (If), an hyperpolarization-activated, inward current that drives diastolic depolarization resulting in spontaneous
activity in cardiac pacemaker cells, are altered during critical illness. Furthermore, membrane channels kinetics
seem to have significant impact upon HRV, whose early decrease might reflect a cellular metabolic stress. In this review
article we present research findings regarding intracardiac origin of HRV, at the cellular level and in both isolated sinoatrial
node and whole ex vivo heart preparations. In addition, we will review results from various experimental studies
that support the interrelation between If and HRV during endotoxemia. We suggest that reduced HRV during sepsis could
also be associated with altered pacemaker cell membrane properties, due to ionic current remodeling.
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