Heart rate variability

Heart rate variability (HRV) is the physiological phenomenon of variation in the time interval between heartbeats. It is measured by the variation in the beat-to-beat interval. Heart rate variability (HRV) is the physiological phenomenon of variation in the time interval between heartbeats. It is measured by the variation in the beat-to-beat interval. Other terms used include: 'cycle length variability', 'RR variability' (where R is a point corresponding to the peak of the QRS complex of the ECG wave; and RR is the interval between successive Rs), and 'heart period variability'. Methods used to detect beats include: ECG, blood pressure,ballistocardiograms,and the pulse wave signal derived from a photoplethysmograph (PPG). ECG is considered superior because it provides a clear waveform, which makes it easier to exclude heartbeats not originating in the sinoatrial node. The term 'NN' is used in place of RR to emphasize the fact that the processed beats are 'normal' beats. Reduced HRV has been shown to be a predictor of mortality after myocardial infarction although others have shown that the information in HRV relevant to acute myocardial infarction survival is fully contained in the mean heart rate.A range of other outcomes and conditions may also be associated with modified (usually lower) HRV, including congestive heart failure, diabetic neuropathy, post–cardiac-transplant depression, susceptibility to SIDS and poor survival in premature babies. There is interest in HRV in the field of psychophysiology. For example, HRV is related to emotional arousal. High-frequency (HF) activity has been found to decrease under conditions of acute time pressure and emotional strain and elevated anxiety state, presumably related to focused attention and motor inhibition. HRV has been shown to be reduced in individuals reporting to worry more. In individuals with post-traumatic stress disorder (PTSD), HRV and its HF component (see below) is reduced whilst the low-frequency (LF) component is elevated. Furthermore, PTSD patients demonstrated no LF or HF reactivity to recalling a traumatic event. The polyvagal theory describes pathways in the autonomic nervous system that mediate HRV. This theory emphasizes the role of heart rate variability in understanding the magnitude and nature of vagal outflow to the heart. This theory decomposes heart rate variability based on frequency domain characteristics with an emphasis on respiratory sinus arrhythmia and its transmission by a neural pathway that is distinct from other components of HRV. There is anatomic and physiological evidence for a polyvagal control of the heart. The neurovisceral integration model describes how the prefrontal cortex regulates activity in limbic structures which act to suppress parasympathetic activity and activate sympathetic circuits. Variation in the output of these two branches of the autonomic system produces HRV and activity in the prefrontal cortex can hence modulate HRV. Variation in the beat-to-beat interval is a physiological phenomenon. The SA node receives several different inputs and the instantaneous heart rate or RR interval and its variation are the results of these inputs. The main inputs are the sympathetic and the parasympathetic nervous system (PSNS) and humoral factors. Respiration gives rise to waves in heart rate mediated primarily via the PSNS, and it is thought that the lag in the baroreceptor feedback loop may give rise to 10 second waves in heart rate (associated with Mayer waves of blood pressure), but this remains controversial.