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Biomedical subjects

O A Beck

Publications and source records attributed to O A Beck.

At least 55 records · Page 3Linked to original sources
PubMed1977

[Initial serum potassium level in relation to cardiac arrhythmias in acute myocardial infarction (author's transl)].

In 565 patients with acute myocardial infarction admitted to a coronary care unit within 12 hours of the onset of symptoms, serum potassium level was determined on admission. The incidence of dysrhythmias occurring during the first 12 hours was referred to the initial serum potassium level. Hypopotassemia (less than or equal to 3.5 mmol/l) was seen in 9.2% and associated with a significantly higher incidence of ventricular arrhythmias in 33% as compared to 18% in the control group. Especially ventricular fibrillation was significantly more frequent in the hypokalaemic (14%) than in the normokalaemic (3%) patients (P less than 0.01). Hyperpotassemia (less than or equal to 5.1 mmol/l) was found in 6% with a higher incidence of second and third degree AV block and left-bundle branch block. This group was much more prone to severe haemodynamic complications and therefore had a bad prognosis with a high clinic mortality of 53%. There was no relation between supraventricular arrhythmias, sinuatrial bradyarrhythmias and intraventricular block other than left bundle branch block to serum potassium level.

Acute Disease↗
PubMed1977

[Effect of sublingual isosorbide dinitrate on hemodynamics in coronary patients with and without congestive heart failure (author's transl)].

In 17 patients with coronary heart disease, hemodynamic measurements were performed before and after sublingual application of 10 mg isosorbide dinitrate (ISDN). 10 patients showed signs of heart failure with pulmonary congestion and a left ventricular filling pressure above 15 mmHg, resting hemodynamics were normal in 7 patients. Eight of the patients with left ventricular failure had sustained acute myocardial infarctions the size of which was assessed by serial determinations of serum creatine phosphokinase. Application of ISDN resulted in a significant decrease of systemic and pulmonary artery pressures and pulmonary capillary wedge and right atrial pressures of patients both with and without left ventricular failure. Cardiac index and stroke index as well as systemic and pulmonary resistances did not change significantly. ISDN did not affect left ventricular stroke work in patients with elevated filling pressures; however, a decrease of normal filling pressures was associated with a decrease of stroke work. Thus, in coronary patients with chronic congestive heart failure, sublingual application of nitrates results in a beneficial hemodynamic unloading. However, if the acute infarct size is taken into account, it can be demonstrated that hemodynamic improvement after ISDN--judged by the relation stroke work/filling pressure--becomes less pronounced with increasing infarct size.

Adult↗
PubMed1976

[Atrial fibrillation and flutter as a complication of acute myocardial infarction (author's transl)].

Among 909 patients with acute myocardial inarction treated in an intensive care unit between 1970 and 1974, atrial flutter and (or) fibrillation occurred in 124 (13.6%). The incidence of these arrhythmias rose with increasing age and predominantly in paroxysmal form (78%). The clinic mortality of patients with arrhythmias was 42%, while in the remaining 785 it was only 26% (P less than 0.001). Patients with atrial fibrillation and (or) flutter had a higher mean age, more frequently cardiac failure (P less than 0.001) - especially in the prognostically unfavourable severe forms with pulmonary oedema (P less than 0.05) and combined right and left heart failure (P less than 0.001) - and other disorders of impulse conduction or formation and chronic arterial hypertension (P less than 0.01).

Age Factors↗
PubMed1976

[Alternating and intermittent bilateral bundle-branch block in acute myocardial infarct with development of total atrioventricular block].

The development of bilateral bundle branch block of various degree in the course of an acute myocardial infarction was demonstrated in a 74-year-old man during continuous ecg-monitoring. Initially there was a tachycardia- and bradycardia-dependent left bundle branch block, followed by a right bundle branch block with second degree type II AV block (Mobitz), and finally complete bilateral bundle branch block with asystole. Different combinations of incomplete block were shown and the presence of type I and type II second degree block within the bundle branches could be demonstrated; Wenckebach periods became indirectly visualized through changes in the AV conduction. This case illustrates the prognostic importance of progressive intraventricular conduction disturbance and reveals the multiplicity and possible mechanisms of conduction defects within the bundle branches.

Acute Disease↗
PubMed1976

[Hemodynamic and electrocardiographic prolonged nitrate effect during frequency load in coronary disease].

Hemodynamic and electrocardiographic analysis during rapid right atrial stimulation was performed before and one, two, and four hours after oral application of longacting nitroglycerin (5 mg) and isosorbide dinitrate (20 mg) in 11 and 9 patients, respectively with coronary heart disease. Atrial stimulation without nitrate induced significant ischemic ST segment depression. Cardiac output showed a small decrease and the mean arterial, pulmonary artery, and pulmonary wedge pressure increased. Isosorbide dinitrate reduced the ischemic reaction by 40% from the first to the fourth hour after application. Cardiac output, stroke volume, aterial, pulmonary artery, and pulmonary wedge pressure also decreased continuously. Nitroglycerin caused a similar reduction of ischemic ST segment depression for two hours. Systolic, diastolic, and mean arterial pressure decreased significantly. Cardiac output, stroke volume, and pulmonary artery pressure remained unchanged. It was concluded that the applied dose of isosorbide dinitrate showed a more extensive longacting effect.

Blood Pressure↗
PubMed1975

[Clinical course and prognosis of acute myocardial infarction in the elderly (author's transl)].

71 of 840 patients admitted to an intensive care unit (I.C.U.) between 1970 and 1974 because of acute myocardial infarction were aged over 80 years. Age was thus an important determinant of infarction and the death-rate rose steeply with age, the hospital death-rate being 61% in those over 80 but only 8.4% in those under 50 years. The high incidence and severity of haemodynamic complications (pulmonary oedema, generalized heart failure, cardiogenic shock) were the main cause of the high death-rate. Supraventricular arrhythmias (atrial flutter and fibrillation) were frequent. Early treatment in an I.C.U. improved prognosis even in the elderly patient, by control of conduction disturbances and other arrhythmias but also by early recognition and treatment of haemodynamic complications.

Acute Disease↗
PubMed1975

[Oral therapy of ectopic cardiac arrhythmias with Propafenon (author's transl)].

The antiarrhythmic effect of Propafenon administered orally in single doses of 600 resp. 900 mg (X = 10,2 Mg/kg/ bodyweight) was examined in 20 patients with chronic and stabile extrasystoles of either ventricular or supraventricular origin. In 18 patients the ectopic beats could be completely eliminated, 2 patients did not respond to antiarrhythmic therapy. The antiarrhythmic effect begins 30 minutes after administration of the drug and has its maximum 3 hours after application with a duration of more than 8 hours in most patients. Propafenon is an effective drug for oral therapy of ectopic cardiac arrhythmias.

Administration, Oral↗
PubMed1975

[Retardation of the excitation conduction by propaphenone. Duration and dosage effect relation after oral administration (author's transl)].

After oral administration, and depending on dosage, propaphenone produces a uniform delay of the excitation conduction in the region of the atrium, ventricle and atrioventricular conduction. At a dosage of 5 or 10 mg/kg body-weight (1 or 2x 300 mg capsules) propaphenone causes an average delay of excitation conduction of + 11% or + 19% of the initial value, and of + 39% (capsule) or + 30% (sugar coated tablet) at 14 mg/kg body-weight. The maximum effect is attained 2.5 to 4 hours after administration. A prolongation of conduction times and consequently of the anti-arrhythmic efficacy, is still found eight hours after oral ingestion.

Administration, Oral↗
PubMed1975

[Long-term action of nitrites in coronary heart disease (author's transl)].

Haemodynamic investigations were performed before and after oral ingestion of nitroglycerine and isosorbide dinitrate, both in depot form, in eleven and nine patients, respectively, with coronary heart disease. Nitroglycerine (5 mg) led to a significant decrease in arterial and pulmonary artery mid-pressure over one to two hours. Heart rate and mean pulmonary capillary pressure as well as cardiac output and stroke volume hardly changed. After ingestion of isosorbide dinitrate (20 mg) there was a continuous and significant fall in mean arterial, pulmonary artery, and pulmonary capillary pressure already demonstrable during the first hour. Cardiac output and left ventricular work decreased accordingly for up to four hours. At the same time the cardiac output remained constantly lowered over four hours despite the significant increase in frequency. Isosorbide dinitrate has thus a more complete and longer lasting protective haemodynamic effect than nitroglycerine.

Blood Pressure↗
PubMed1975

[Effect of aprotinin in acute myocardial infarction (clinical double-bind study (author's transl)].

In a double-bind study 164 patients with acute myocardial infarction, admitted to an intensive-care unit within 72 hours of infarction, were randomly treated for three days either with aprotinin (Trasylol-82 persons) or placebo (82 persons). Retrospective analysis proved both patient groups to have been comparable in all other respects. There was no definite influence on the course of the infarction, haemodynamic changes, arrythmias or mortality rate. Trasylol thus has no therapeutic importance in the treatment of acute myocardial infarction.

Acute Disease↗
PubMed1975

[Propafenon, a new antiarrhythmic agent for the treatment of ectopic and rapid cardiac arrhythmias (author's transl)].

Propafenon (SA 79, Fenoprain, Baxarytmon) is a new antiarrhythmic agent with "quinidine-like" localanaesthetic direct membrane and beta adrenergic blocking actions. The drug was given to 50 patients with various types of cardiac arrhythmias. The effective and compatible dose was 70-140 mg administered intravenously in 1 to 3 minutes. Therapeutic success was observed in ectopic beats and paroxysmal tachycardias of both atrial and ventricular origin. Propafenon is effective on the sinus node, the atrial wall and the atrioventricular muscle; the rate of sinus node and ectopic pacemakers is lowered. The atrioventricular and intraventricular conduction time may be increased. Within the therapeutic dose Propafenon has only minimal cardiodepressive activity. Propafenon should not be given in patients with severe heart failure, hypotension and shock and atrioventricular block.

Adrenergic beta-Antagonists↗
PubMed1975

[Acute effect of lidoflazine on the electrocardiographic agitation discharge in atrial frequency stimulation (studies on patients with stress-induced coronary insufficiency)].

Electrocardiographic alterations and onset of angina pectoris during an acute treatment period with lidoflazine -3 to 4 mg/kg b.w. by oral application- was investigated in 20 patients with latent coronary insufficiency under increasing heart rate condition by atrial pacing. Significant changes in the repolarisation phase mainly due to prolongation of the QTc-interval already appeared 90 to 120 min after oral administration. The onset of test-induced agina pectoris and ischaemic ST-segmental depression in the ECG were not influenced by lidoflazine. Exceeding a rate of 140 min-1 produced a delay of atrioventricular conduction time under drug influence whereas significant changes of intraventricular conduction did not appear. Under frequent heart rates bundle branch block developed in a few individuals that might be drug-induced. In addition, there were some signs of digitalis-potentiation by lidoflazine.

Administration, Oral↗
PubMed1975

[Effect of the antiarrhythmic agent propaphenone on cardiac conduction. clinical studies using bundle of his electrography].

The influence of the new antiarrhythmic agent Propafenon on cardiac conduction and sinus node function was studied by using His-bundle recordings and atrial stimulation in 14 patients with normal and diseases conduction system. Intravenous administration of Propafenon in therapeutic dose (1-2 mg/kg) produced a significant prolongation of the atrioventricular conduction time. Increase of the A-H interval was observed in 13 of 14 subjects during sinus rhythm. Second degree A-V block (Wenckebach form) during atrial stimulation occurred at lower frequencies after administration of the drug. The impulse propagagion within the His-Purkinje system was depressed significantly (H-V interval in 8, H-S interval in 10 of 14 subjects). Propafenon did not cause any alteration in intraatrial conduction, but depression of the sinus node automaticity was noted. Total reversal of the drug induced prolonged atrioventricular conduction and a decrease of the sinus rate was seen after administration of orciprenaline. Beta-adrenergic receptor blocking and local anaesthetic direct membrane actions are discussed as possible cause of the prolongation of atrioventricular and intraventricular conduction.

Adrenergic beta-Antagonists↗