Heart Rate Variability: for real doctors. Regulation in the disease. Accents on low Total Power of HRV

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.

9. Regulation in the disease

Accents on low Total Power of HRV

Low Total Power (TP) of HRV often associates with high heart rate (HR), and that is why HR is one of the critical characteristics of HRV and regulation in general.
HR reflects not only heart function but the condition of regulation in general too.
Increased HR at baseline reflects decreased health from simple physical detraining up to severe diseases.
The higher HR always means lower health.
High HR is a consequence and a satellite most diseases of cardiovascular system, first of all, arterial hypertension, ischemic heart disease, myocarditis, cardiomyopathy, heart defects.
High HR often is the result of a somatoform disturbance, endocrine deviations, in the first line of thyroid hyperfunction.
High HR means a chronic obstructive pulmonary disease, one of the central nervous system diseases, systemic diseases of connective tissue.
High HR means a chronic obstructive pulmonary disease, one of the central nervous system diseases, systemic diseases of connective tissue, chronic infectious diseases (sepsis, tuberculosis, angina, etc.), anemia and a lot of other pathological conditions.
At least increased HR can be a result of medicinal intoxication.
HR carries function as one of the indicators of the heart, and at first look, it is so.
Natural dominant heart pacemaker or a sinus node situates in the heart. In physiological condition at rest, it supports HR in diapason 60-100 beats per minute.
But extracardiac structures, not the heart, define HR.
Sympathetic stimulation and parasympathetic depression is the direct mechanism of HR increase.
In healthy HR of rest is nor higher than the average level of the norm, and increases due to stress with a quick return to the base level.
If HR is high normal, its increase on stress is no adequately mightily, and after that, it restores slow or no fully, you should think at least about of physical detraining if no about the pre-illness or even illness.
Every one of these conditions is no physiologically normal.
In patients, everything changes in another way. Systemic mechanisms of the disease realize through chronic pathological over stress or distress that in the clinic names as general adaptation syndrome.
One of the main effects of the general adaptation syndrome is sympathetic overactivation that manifests with increased base HR and over strengthening in all life processes. As a result, a decrease in health, instability and dramatically increased the risk of fatal cataclysms that demand emergency actions.
The most seak place in general adaptation syndrome is the cardiovascular system.
Chronic distress with sympathetic hyperactivation is the main factor of decreased quality of health, diseases development, and even sudden cardiac death.
The direct cause of sudden cardiac death in case of sympathetic hyperactivation is electrical nonstability of heart with the high risk of fatal ventricular tachycardias up to fibrillation.
Chronic distress is no ordinary distress but nuclear part of arterial hypertension, ischemic heart disease, coronary brain disease, and other fatal vascular diseases.
Between key players of weak link situated increased base HR, that reflects the following information about human health:
• decreased health level
• pure physical shape
• chronic sympathetic distress
• accelerated metabolic processes
• high risk of development and weighting arterial hypertension
• high risk of acute ischemic attacks in vascular pools of the heart and brain, chronic vascular heart and brain insufficiencies and other complications of systemic atherosclerosis
• disturbance in phase structure of heart cycle with diastole shortening and development dystrophic processes in the heart
• sclerotic changes in the heart with trouble in it contractile function
• Threshold decrease for lethal ventricular tachycardia as the most common mechanisms of cardiac death
• an increase of peripheral resistance and mechanical overload on the heart
• increase in systolic in diastolic blood pressure
• development or progression of heart failure
• secondary changes in other organs and systems
• a compensatory mechanism at vegetative disturbances as at hemodynamic disturbances
• lower qualitative and more difficult short life.
The most effective drugs for high heart rate are beta-adrenergic receptor blockers. In the case of paroxysm, a rise in the resting heart rate is used by short-range medications. A steady, chronic increase in heart rate requires long-acting drugs.
Beta-adrenergic receptor blockers are the only group of drugs that:
1. improve the quality of life
2. increase the lifespan,
3. reduce the risk and frequency of fatal ventricular arrhythmias,
4. reduce the risk and frequency of acute ischemic attacks in the vascular
basins of the heart and brain,
5. cut the risk and incidence of recurrent coronary and vascular
brain events
6. lower blood pressure,
7. optimize frequency-adaptive blood pressure reactions during
8. lower resting heart rate,
9. optimize the frequency-adaptive response of the heart rate at voltage.
During HR acceleration, life becomes heavier and shortens in most diseases. The unusually strong increase in heart rate affects life expectancy in patients with arterial hypertension and coronary artery disease. Heart rate is a predictor of death, illness, and quality of health.

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