RR Intervals, Heart Rate, and HRV Howto
the variability of RR intervals is higher for the slow average heart rate than for the (B) the relationship between RR interval and heart rate with two hypothetical. There is an inverse correlation between the HRV and HR: a larger HRV (R-R interval) was correlated with a lower HR, and the vice versa. QT interval*, Total duration of ventricular depolarization (all myocytes), up to sec (must be corrected for heart rate). R-R interval (heart rate)*, Time between.
Physiological correlates of HRV components[ edit ] Autonomic influences of heart rate[ edit ] Although cardiac automaticity is intrinsic to various pacemaker tissues, heart rate and rhythm are largely under the control of the autonomic nervous system. The parasympathetic influence on heart rate is mediated via release of acetylcholine by the vagus nerve.
Acetylcholine also inhibits the hyperpolarization-activated "pacemaker" current. The "Ik decay" hypothesis proposes that pacemaker depolarization results from slow deactivation of the delayed rectifier current, Ik, which, due to a time-independent background inward current, causes diastolic depolarization.
Conversely, the "If activation" hypothesis suggests that after action potential termination, If provides a slowly activating inward current predominating over decaying Ik, thus initiating slow diastolic depolarization. The sympathetic influence on heart rate is mediated by release of epinephrine and norepinephrine.
Under resting conditions, vagal tone prevails and variations in heart period are largely dependent on vagal modulation. The vagal and sympathetic activity constantly interact. Because the sinus node is rich in acetylcholinesterase, the effect of any vagal impulse is brief because the acetylcholine is rapidly hydrolyzed. Parasympathetic influences exceed sympathetic effects probably through two independent mechanisms: Components[ edit ] The RR interval variations present during resting conditions represent beat-by-beat variations in cardiac autonomic inputs.
However, efferent vagal parasympathetic activity is a major contributor to the HF component, as seen in clinical and experimental observations of autonomic maneuvers such as electrical vagal stimulation, muscarinic receptor blockade, and vagotomy.
More problematic is the interpretation of the LF component, which was considered by some as a marker of sympathetic modulation especially when expressed in normalized units but is now known to include both sympathetic and vagal influences.
For example, during sympathetic activation the resulting tachycardia is usually accompanied by a marked reduction in total power, whereas the reverse occurs during vagal activation. Thus the spectral components change in the same direction and do not indicate that LF faithfully reflects sympathetic effects. It is important to note that HRV measures fluctuations in autonomic inputs to the heart rather than the mean level of autonomic inputs.
Thus, both withdrawal and saturatingly high levels of autonomic input to the heart can lead to diminished HRV. Changes related to specific pathologies[ edit ] A reduction of HRV has been reported in several cardiovascular and noncardiovascular diseases. HRV in patients surviving an acute MI reveal a reduction in total and in the individual power of spectral components. The presence of an alteration in neural control is also reflected in a blunting of day-night variations of RR interval.
Diabetic neuropathy[ edit ] In neuropathy associated with diabetes mellitus characterized by alteration in small nerve fibers, a reduction in time domain parameters of HRV seems not only to carry negative prognostic value but also to precede the clinical expression of autonomic neuropathy.
EKG Interpretive skills
In diabetic patients without evidence of autonomic neuropathy, reduction of the absolute power of LF and HF during controlled conditions was also reported. Similarly, diabetic patients can be differentiated from normal controls on the basis of reduction in HRV. The appearance of discrete spectral components in a few patients is considered to reflect cardiac reinnervation.
This reinnervation may occur as early as 1 to 2 years after transplantation and is assumed to be of sympathetic origin. In addition, a correlation between respiratory rate and the HF component of HRV observed in some transplanted patients also indicates that a nonneural mechanism may generate a respiration-related rhythmic oscillation. Myocardial dysfunction[ edit ] A reduced HRV has been observed consistently in patients with cardiac failure.
In this condition characterized by signs of sympathetic activation such as faster heart rates and high levels of circulating catecholamines, a relation between changes in HRV and the extent of left ventricular dysfunction was reported.
In fact, whereas the reduction in time domain measures of HRV seemed to parallel the severity of the disease, the relationship between spectral components and indices of ventricular dysfunction appears to be more complex. In particular, in most patients with a very advanced phase of the disease and with a drastic reduction in HRV, an LF component could not be detected despite the clinical signs of sympathetic activation.
This reflects that, as stated above, the LF may not accurately reflect cardiac sympathetic tone.
Heart rate variability
Liver cirrhosis[ edit ] Liver cirrhosis is associated with decreased HRV. Decreased HRV in patients with cirrhosis has a prognostic value and predicts mortality. Loss of HRV is also associated with higher plasma pro-inflammatory cytokine levels and impaired neurocognitive function in this patient population. Loss of HRV has both diagnostic and prognostic value in neonates with sepsis. However, an LF component can be detected in HRV and arterial pressure variabilities of some tetraplegic patients.
Thus, the LF component of HRV in those without intact sympathetic inputs to the heart represent vagal modulation. Sudden cardiac death[ edit ] Patients victim of sudden cardiac death have been found to have lower HRV than healthy individuals.
Although the rationale for changing HRV is sound, it also contains the inherent danger of leading to the unwarranted assumption that modification of HRV translates directly into cardiac protection, which may not be the case. Despite the growing consensus that increases in vagal activity can be beneficial, it is not as yet known how much vagal activity or HRV as a marker has to increase in order to provide adequate protection.
Despite the observation of statistically significant increases, the actual changes are very modest. Antiarrhythmic drugs[ edit ] Data exist for several antiarrhythmic drugs. Flecainide and propafenone but not amiodarone were reported to decrease time domain measures of HRV in patients with chronic ventricular arrhythmia.
A larger study confirmed that flecainide, also encainide and moricizine, decreased HRV in post-MI patients but found no correlation between the change in HRV and mortality during follow-up. Thus, some antiarrhythmic drugs associated with increased mortality can reduce HRV.
However, it is not known whether these changes in HRV have any direct prognostic significance. Scopolamine[ edit ] Low-dose muscarinic receptor blockers, such as atropine and scopolamine, may produce a paradoxical increase in vagal effects on the heart, as suggested by a decrease in heart rate.
In addition, scopolamine and low dose atropine can markedly increase HRV. However, though the heart rate slowing in proportional to the low dose of atropine, the increase in HRV varies widely across and within individuals. This suggests that even for vagal activity to the heart, HRV may be a limited marker. HRV was higher 90 minutes after thrombolysis in the patients with patency of the infarct-related artery.
However, this difference was no longer evident when the entire 24 hours were analyzed. Exercise training[ edit ] Exercise training may decrease cardiovascular mortality and sudden cardiac death. Regular exercise training is also thought to modify cardiac autonomic control. Individuals who exercise regularly have a 'training bradycardia' i.
RR Intervals, Heart Rate, and HRV Howto
Biofeedback[ edit ] The technique called resonant breathing biofeedback teaches how to recognize and control involuntary heart rate variability. A randomized study by Sutarto et al. Abstract The dynamical fluctuations in the rhythms of biological systems provide valuable information about the underlying functioning of these systems. During the past few decades analysis of cardiac function based on the heart rate variability HRV; variation in R wave to R wave intervals has attracted great attention, resulting in more than publications PubMed list.
However, it is still controversial about the underling mechanisms of HRV. In this study, we performed both linear time domain and frequency domain and nonlinear analysis of HRV data acquired from humans and animals to identify the relationship between HRV and heart rate HR. The HRV data consists of the following groups: In both human and animal data at variant pathological conditions, both linear and nonlinear analysis techniques showed an inverse correlation between HRV and HR, supporting the concept that HRV is dependent on HR, and therefore, HRV cannot be used in an ordinary manner to analyse autonomic nerve activity of a heart.
Introduction Greek Physicians and scientists were the pioneers who measured pulse rate; however, it was not much accurate till the invention of pulse watch in [ 1 ]. The correlation between heart rate variability, blood pressure and respiratory rate was first observed by Stephen Hales in [ 1 ].
His observation was confirmed by Carl Ludwig in [ 1 ], who noted increase in heart rate and blood pressure with inspiration and a decrease in these two parameters with expiration. The advances in digital signal processing techniques and long term ambulatory ECG recording opened a new arena for HRV analysis and its linkages to health and disease [ 1 ]. The study of heart rate variability HRV is a research area that has attracted more and more researchers, causing significant increase in the number of publications in this field.
According to PubMed present list of publications in this research area exceeds research articles [ 2 ]. Heart Rate Variability HRV analysis is a non-invasive technique used to evaluate the balancing action of sympathetic and parasympathetic branches of the autonomic nervous system [ 345 ]. Over the last four decades advances in the data acquisition systems and their associated computational tools have resulted into fast and robust application methods to extract valuable information from heart rate signals.
HRV reflects the cardiac autonomic control of the ANS and its measurement can provide additional information about the controlling mechanism of ANS compared to the measurements of heart rate alone. Over the last 35 years, various linear and non-linear techniques have been developed to extract the valuable information from cardiac interbeat interval time series data, aiming to help clinician for prognostication of illness and assessing malfunctioning of the autonomic nervous system.
However, often contradictory results have left clinicians skeptical and there exists no clear consensus about HRV analysis measures [ 6 ].