From Big Medical Encyclopedia

CORDIAL AND VASCULAR INSUFFICIENCY — the morbid condition which is characterized by a combination of the main pathogenetic signs and clinical symptoms of heart and vascular failure. Etiological factors of heart and vascular failure can be various (see. Heart failure , Vascular insufficiency ).

Domestic cardiologists G. F. Lang, A. L. Myasnikov accurately differentiated heart and vascular failure, specifying that cardinal pathogenetic mechanisms and the main symptoms of these states, as a rule, are mutually exclusive owing to the fact that heart failure is characterized by decrease in contractility of a myocardium, and vascular insufficiency — decrease in a tone of vessels. S.'s identification which is quite often found in special literature - page of N and heart failure in essence to the is wrong.

The page - page of N can sharply develop or have a chronic current.

The most common causes of acute S. - page of N — extensive myocardial infarction (see), an embolism of large branches of a pulmonary trunk (see. Embolism of a pulmonary artery ), obstruction of the left atrioventricular opening spherical blood clot, cardiac tamponade (see), not sinus tachycardia with very high frequency of cordial reductions, napr, an atrial flutter 1:1 (see. Ciliary arrhythmia ), nek-ry forms Bouveret's disease (see). The combination of the heart failure caused by infectious is sometimes observed myocarditis (see), with collapse (see), caused by the same infection. S.'s development - page of N at the myocardial infarction and other morbid conditions leading to sharp reduction of cordial emission happens, apparently, in connection with a hypoxia of a vasomotor center and walls of peripheral vessels, and also owing to exhaustion of reactivity of vascular walls on pressor influences. It is known that at cardiogenic shock (see) the first minutes or hours arterial pressure decreases not owing to vascular insufficiency, and only in connection with falloff of cordial emission whereas the tone of vessels does not decrease, and sometimes even increases a little; thus, vascular insufficiency during this period is absent. Further, if it is not possible to bring the patient out of shock, vascular insufficiency joins what falling of the general peripheric vascular resistance testifies to. Other important mechanism of development of acute S. - the page of N serves the so-called unloading reflex described by V. V. Larin and H. Schwiegk consisting in decrease in arterial, venous pressure and delay of rate of cordial reductions at an acute overload of a pulmonary circle of blood circulation. In physiological conditions this reflex protects from an overload the right departments of heart at supertension in system of a pulmonary trunk, but at nek-ry forms of pathology, napr, at an embolism in system of a pulmonary trunk, it promotes acute S.'s development - page of N. The cordial component of acute S. - page of N can carry both left-(myocardial infarction), and right ventricular (an embolism in system of a pulmonary trunk) character; at a cardiac tamponade there is total heart failure.

Chronic heart failure (see) in most cases is not followed by vascular insufficiency; on the contrary, with increase of heart failure owing to vasoconstriction the general peripheric resistance increases; only in an end-stage the irreversible collapse develops. Chronic S. - page of N arises when the same pathogenic factor it is long influences a myocardium and smooth muscle elements of a vascular wall; most often it is observed at thyrotoxicosis (see), beriberi (see) and anemias (see). Characteristic pathogenetic features in these cases are decrease in peripheric vascular resistance and increase in cordial emission. Thus, development of a cordial component C. - page of N is promoted by an overload of heart volume. It was suggested that the overload volume is not enough for development of heart failure and that it appears at a hyperthyroidism and anemia only when heart is affected with some accompanying pathological process [Fridberg (S. K. of Friedberg)]. However it is established that even at healthy heart the overload volume can lead to development of heart failure that is observed, e.g., at patients with a large arteriovenous anastomosis. In all cases hron. The page - page of N is available the dystrophy of a myocardium (connected at a thyrotoxicosis it is a lot of hormones of a thyroid gland, at beriberi — with deficit of vitamin of Vkh, at anemia — with a hypoxia).

Acute S.'s treatment - page of N is extremely complicated as the most part of the funds allocated for fight against heart failure promotes development of vascular insufficiency, and, on the contrary, the means raising a tone of vessels aggravate displays of heart failure. Appoint the cardiac glycosides (which are not reducing a vascular tone), the diuretics which are not possessing the expressed hypotensive action (e.g., lasixum intravenously). At an opportunity carry out causal treatment (a lysis of the blood clot which is in arteries of system of a pulmonary trunk or its surgical removal). At hron. The page - page of N is effective only etiological (a thyroidectomy at a diffusion toxic craw, administration of thiamin at beriberi) or pathogenetic treatment (hemotransfusion, completion of deficit of iron, stimulation of a hemopoiesis at anemias).

Bibliography: Johnson P. Peripheric circulation, the lane with English, M., 1982; Zelenin V. F. Diseases of cardiovascular system, M., 1956; Lang G. F. Diseases of the blood circulatory system, M., 1957; Nesterov V. S. Clinic of heart troubles and vessels, Kiev, 1974; Pokrovsky A. V. Clinical angiology, M., 1979; Preventive cardiology, under the editorship of G. I. Kosits-ky, M., 1977; Rashmer R. Dynamics of cardiovascular system, the lane with English, M., 1981; The Guide to cardiology, under the editorship of E. I. Chazova, t. 1 — 4, M., 1982; Evans E. Carotid sinus, its clinical importance, J. Amer. med. Ass., v. 149, p. 46, 1952; Perrannini A. Constitutional angiohypotony, or idiopathic permanent arteriohypotension, Lancet, v. 1, p. 1131, 1931; Heinrich F. Therapie der Hypotonien, Med. Welt (Berl.), S. 571, 1972; Laberke J. A. Zur Genese und Therapie der hypotonen Regulationsstorun-gen, Dtsch. med. Wschr., S. 133, 1952; Page I. H. a. o. Blood pressure reducing property of extracts of kidneys in hypertensive patients and animals, Ann. intern. Med., v. 15, p. 347, 1941; S v a r t z N. Hypotonie als isoliertes Symptom, Schweiz, med. Wschr., S. 922, 1953; Weidinger P. u. Stein-b a with h K. Diagnostische und therapeu-tische Moglichkeiten beim Orthostasesynd-rom, Wien. Z. inn. Med., S. 490, 1973.

V. A. Bogoslovsky.