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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The changes in the basic hemdynamic indices and in the phase structure of the cardiac cycle in patients with acute infarction prior to and post treatment with beta-blockers (Obsidan and Trasicor) were studied. Manifested changes in the hemodynamics were established, namly: pulse rate and cardiac flow decrease, the total peripheral resistance grows; veloqcilty of blood flow is slowed down. The preparations used have a negative effect upon the phase structure of left ventricle as well. The authors underline that beta-blockers administration in acute myocardial infarction should be evaluated very carefully and in the presence of clinical signs for cardiac insufficiency, it should be carried out on the background of cardiotonic treatment.
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PMID:[Changes in myocardial contractile function and in the hemodynamic indices in patients with myocardial infarct before and after beta-blockader treatment]. 35 4

The observation was conducted in 92 patients with rhythm and conductivity disorders induced by cardiac glycosides. Most of the patients had ischaemic heart disease, 60 of them having had acute myocardial infarction. All patients were prescribed cardiac glycosides (usually Strophantin and digitalis preparations) due to the appearance of cardiac insufficiency. The most frequently observed rhythm disorder consisted in ventricular extrasystole (69.5% of the cases), bigeminy, polytopic or group extrasystole being observed in many cases. Often arrhythmias consisted in atrial extrasystole, atrial fibrillation, atrial and ventricular tachycardia, atrioventricular block. "Digitalis" arrhythmias were treated with beta-adrenergic blockers: Inderal, Viskene, Eraldin, Trasicor and Aptin. These drugs proved effective in most cases with atrial arrhythmias and in some--with ventricular arrhythmias. Lidocain was more effective in cases of ventricular arrhythmias. Effective drugs of a broad spectrum are also Aimalin, Pulsenorma and Ritmodan.
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PMID:["Digitalis" arrhythmias and their treatment]. 101 1

The paper presents the results of an examination of 62 patients with postinfarction cardiosclerosis by means of echocardiography and ultrasonic scanning. The impact of the asynergy zone on the development of cardiac insufficiency was studied with reference to the area of myocardial lesion. Myocardial hyperkinesia is characterized, its compensatory effect in postinfarction cardiosclerosis and arterial hypertension is discussed. The effect of Inderal and Ildomen on both the zones of hyperkinesia, and on the indices of cardiac haemodynamics as a whole is described.
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PMID:[Importance of myocardial asynergy zones in the development of cardiac insufficiency]. 101 9

Changes in the duration and size of the vulnerable period of the myocardium in the presence of respiratory changes were studied in acute experiments on rats. The limits of the vulnerable period were determined by directly stimulating the heart during ventilation via the enlarged respiratory dead space, during hyperventilation and during heart failure. In the control group (normal ventilation without enlargement of the dead space), the vulnerable period lasted 5.7 +/- 0.76 ms. During ventilation via the enlarged dead space, hypercapnic hypoxaemia developed and the vulnerable period was markedly prolonged (18.55 +/- 5.29 ms) by a shift of its inner limit to the left. Hyperventilation caused normoxic to hyperoxic hypocapnia and markedly reduced the duration of the vulnerable period (8.17 +/- 2.21 and 9.31 +/- 2.38 ms respectively). The vulnerable period lengthened the most in heart failure (25.46 +/- 3.93), mainly as a result of a shift of its outer limit. In all the experimental groups there was a shift of the vulnerable period to the right, which was fastest in hypercapnic hypoxaemia and slowest in hyperoxic hypocapnia. The administration of Inderal (3 mg/kg i.p.) or Arfonad (50 mg/kg i.p.) markedly shortened the vulnerable period during hypercapnic hypoxaemia (9.87 +/- 2.78 and 9.32 +/- 2.16 ms respectively), but did not block the shift. Lengthening of the vulnerable period during hypercapnic hypoxaemia was probably due to activation of sympathetic nerves via beta-adrenergic receptors.
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PMID:Changes in the vulnerable period of the rat myocardium during hypoxia, hyperventilation and heart failure. 643 69