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
Some pathological conditions
Heart failure. There are two main variants of changes in HRV, on which the prognosis for the life of patients depends.
When two abnormal areas of high density of RR-intervals appear on the scattergram with a decrease in the variability of their lengths, heart failure is accompanied by a high level of blood epinephrine.
When a high variability of the lengths of RR-intervals without local condensation is preserved on the scattergram, the level of blood epinephrine is normal.
The first option is prognostically less favorable and carries the danger of sudden death.
Patients with unexpressed mid-frequency activity (not expressed LF peak), belonging to the first group of HF, have a smaller average length of RR-intervals and SD, a high concentration of plasma epinephrine.
The reason for the decrease in HRV in most patients is a drop in parasympathetic tone.
Its degree directly correlates with the severity of left ventricular dysfunction.
It is for these reasons that the high risk of ventricular arrhythmias and poor prognosis is largely explained.
Reduced HRV is a predictor of high mortality and in severe heart failure.
The higher is the class, the less HRV.
Signs of a stable condition of patients with HF are the maintenance of HRV indices at the same level on a long time interval (at least 6 months).
The predominance of sympathetic tone reflects the blockade of beta-adrenergic receptors, induced by a decrease in HRV.
ACE blockers have a very favorable effect on the structure of HRV in patients.
It is believed that these drugs contribute to reducing the mortality of patients with heart failure.
In decompensated patients with dyspnea, HRV modulation occurs and the HF peak in the frequency range corresponding to the frequencies of modulated respiration is determined on the spectrogram.
“Degeneration” of the high-frequency element of the overall spectrum of HRV in heart failure.
The patient is 47 years old. Tachycardic dilatation of the left ventricle, HF FC III, sinus tachycardia (107 beats/min), slight arterial hypertension (140/100 mm Hg), the absence of frequency-adaptation reactions. HRV – at the top in laying position and below – in orthostasis. A sharp drop in the TP of the HRV spectrum with a “degeneration” of the power of the HF. Providing an orthostatic reaction due to the LF of HRV. An extreme case of dysregulation.
Patient, 59 years old. CHD: Stable exertional angina III FC. Postinfarction cardiosclerosis. Q-myocardial infarction of the anterior wall of the left ventricle (2000, 2003). HF FC III. Prior to the onset of therapy, blood pressure is 100/70 mm Hg, heart rate is 67 beats/min, after 3 months of therapy with carvedilol, aspirin, ACE inhibitors, and statins blood pressure is 110/70 mm Hg, HR is 66 beats/min. Left data before and right – after 3 months of therapy. Prior to the initiation of therapy, the low TP of the HRV spectrum, the predominance of slow- and mid-frequency links of the HRV spectrum. After therapy, the tendency is to improve the spectral indices of HRV.