Heart Rate Variability: for real doctors. What is Heart Rate Variability (HRV) and why is it a window into human regulatory systems? Organizing non-cardiac regulatory systems

Yabluchansky N.I., Martynenko A.V.

Heart rate variability: for real doctors. Translation from the Russian version of the book, published at Kharkiv, 2010, 131 p.
The basics and practice of the clinical use of the technology of heart rate variability are outlined for doctors of all specialties and students of medical faculties of universities.

What is Heart Rate Variability (HRV) and why is it a window into human regulatory systems?

Physiological functions including the blood circulation in their temporary organization are periodic processes. The periodic nature of the blood circulation is generated by the cyclic organization of the heart contractions.
The length of the cardiac cycle is its period. The value inverse to it, which is more convenient and therefore is more often used in practice, is heart rate (HR).
The doctor counts HR per 1 minute.

In our case, if it is not specifically mentioned, HR is understood precisely as a value inverse to the length of the concrete cardiac cycle, or in other words as an instantaneous HR. Expressed in HR per 1 minute, it shows what the heart rate would be for 1 minute, provided that all consecutive heart cycles have the same duration.
Changes in HR from cycle to cycle are the result of its multi-contour, multi-level hierarchical non-linear control by regulatory systems, including in the broad sense, vegetative and humoral regulation.
Through the sight, hearing, and another exteroreceptors regulation is open to the surrounding world. The man in his whole being is inextricably linked with the world around him and is his or her integral part for the entire period of the life. That is why in HR lies information about the state of regulation, its quality, including concerning ensuring unity of relations with the surrounding world, and the method that allows evaluating this regulation has been called the HRV technology.

Organizing non-cardiac regulatory systems
The fastest link in the management of HR is an autonomous nervous system (ANS) that acts under the control of the central nervous system (CNS). Its highest vegetative centers localize in the under cortical structures, brainstem, spinal cord and have representation in the motor, premotor and orbital zones of the cortex. These centers perform the function of vegetosomatic and vegetomotivational integration. The hypothalamus that associated with the cortex, brainstem and spinal cord controls unconditional and conditional-reflective regulation of respiration, blood circulation, metabolism, and other functions.
The brainstem with its vagal nuclei gives the vagus nerves that are a part of the parasympathetic nervous system (PSNS). The other centers of the system localize in thoracolumbar and sacral zones of the spinal cord.
Sympathetic nuclei of the sympathetic nervous system (SNS) localize in the lateral grey columns of thoracolumbar zones of the spinal cord. Their cell bodies are the preganglionic neurons. The locations upon which preganglionic neurons can synapse for their postganglionic neurons are paravertebral ganglia of the sympathetic chains, prevertebral ganglia, and chromaffin cells of the adrenal medulla. These ganglia provide the postganglionic neurons from which innervation of target organs follows. These all contain afferent sensory nerves as well, known as general visceral afferent neurons.
The vagus nerves innervate the heart from the brainstem, and the sympathetic nerves innervate it from the thoracolumbar vegetative centers.
Parasympathetic innervation is less than sympathetic in its prevalence. Some organs have double innervation, and the others have only sympathetic.
SNA is part of the sympathoadrenal system, which includes the medulla of the adrenal glands and other clusters of chromaffin cells. A large number of them localize in the heart.
Stimulation of the SNS leads to an increase in the strength and frequency of heart contractions, acceleration of excitation through the cardiac conduction system and contractile myocardium, increase in blood pressure, causes vasodilation of the heart vessels and vasoconstriction of them in other organs. The sympathetic effects on the heart are mediated by the release of adrenaline and noradrenaline with the activation of beta-adrenergic receptors. The result is an acceleration of slow diastolic repolarization. Stimulation of PSNS has the opposite effects. The release of acetylcholine mediates its effects on the heart rhythm.
The nuclei of the vagus nerves are located close to the respiratory nuclei and therefore are under their influence. Activation of the respiratory nuclei, for example, by metronization of the respiratory rate, has a stimulating effect on the nuclei of the vagus nerves and the PSN activity increases.
In humans, the activity of the ventricles of the heart is mainly under the control of the sympathetic nerves, and the activity of the atria and the sinus node is under the control of sympathetic and parasympathetic nerves. Vessels are subject to sympathetic innervation. PSNS has no direct effect on them, but the multi-level connections of both subsystems of ANS provide an indirect impact of PSN on blood pressure and vascular tone.
Medium and short-term components of regulation (seconds, minutes, tens of minutes) are associated with PSNS and SNS. PSNS and SNA innervation of different parts of the heart is heterogeneous and asymmetrical.
The current activity of PSNS and SNS is the result of a systemic response of multi-loop and multi-level regulation mechanisms. At rest, the tone of the PSN dominates, and variations in a cardiac period largely depend on vagal modulation. The prevalence of the effects of PSN over the SNA can be explained by two independent mechanisms: a cholinergically induced decrease in the release of norepinephrine in response to sympathetic stimulation and a cholinergic suppression of the reaction to an adrenergic stimulus.
Among the humoral systems, the most studied are a hormonal, angiotensin-renin, kallikrein-kinin system, and some others. Their effects on HRV, compared with vegetative, are long-term and occupied the minutes and hours.
Heart rate variability (HRV) is a combination of all its properties, from the changes in instant heart rate, and until its causes, determined by a nonlinearity of sympathetic, parasympathetic, and humoral regulation, their ramified connections between each other, and systemic reactions on different types of stress.


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