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

The CO2 rebreathing cardiac output method is a totally noninvasive Fick procedure needing validation in various disease states to become clinically applicable. Simultaneous measurements of cardiac output by CO2 rebreathing and dye-dilution or direct Fick techniques were performed in 53 patients. In nine patients with pulmonary disease rebreathing cardiac output averaged 4.85 L/min compared to 5.18 L/min by dye-dilution or Fick (r = 0.16). In 14 instances of acute myocardial infarction cardiac output was 5.53 L/min by rebreathing and 5.87 L/min by dye-dilution (r = 0.95), while in nine shock cases it averaged 3.98 L/min by dye-dilution or Fick and 3.75 L/min by CO2 rebreathing (r = 0.94). In five heart failure cases with mitral insufficiency, which may distort dye durves, correlation between standard and rebreathing methods was r = 0.09, but in 16 cases without mitral regurgitation, r = 0.89. Acute interventions in ten patients increased dye-dilution cardiac output by 0.92 L/min and rebreathing outputs by 0.60 L/min (r = 0.87). The data suggest that the CO2 rebreathing cardiac output method may be useful in the CCU-MICU setting.
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PMID:Evaluation of the CO2 rebreathing cardiac output method in seriously ill patients. 31 21

Echocardiographic findings in patients with ischemic heart disease are described; their correlations with clinical, hemodynamic and angiographic data are presented and discussed. Regional abnormalities of left ventricular wall motion and/or thickening during systole are detected in 84 per cent of patients with acute myocardial infarction and in a high percentage of patients with larger than or equal to 75 per cent narrowing of a major coronary artery. These abnormalities may occur with stress and may be reversible. Left ventricular wall thinning during systole indicates acute ischemia or infarction and thin, dense myocardial echoes indicate scar. Echocardiographic evidence of left ventricular dysfunction is useful in predicting heart failure and mortality in patients with acute myocardial infarction and in predicting surgical mortality for patients undergoing aneurysmectomy and/or coronary artery bypass surgery. Echocardiography has not proved useful in determining graft patency following coronary artery bypass surgery. Technical difficulties and limitations of echocardiography in patients with coronary artery disease are discussed.
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PMID:Echocardiography in ischemic heart disease. 32 1

The effect of dopamine was tested in 20 patients with cardiogenic shock. 14 patients suffered from acute myocardial infarction, 6 patients from severe heart failure. In the beginning the dosis of dopamine was 200 to 300 microgram/min. 4 patients with an acute myocardial infarction died in shock. The remaining 10 patients survived the first shock symptomes. All patients with heart failure survived the cardiogenic shock. Hemodynamic studies showed a sigificant increase of the arterial mean pressure and a decrease of the diastolic arterial pulmonary pressure. During dopamine a statistically not significant increase of cardiac index and stroke volume was observed.
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PMID:[Dopamine in patients with cardiogenic shock (author's transl)]. 32 88

A multicentre study of cases of acute myocardial infarction was undertaken at 27 departments at teaching and non-teaching hospitals throughout Austria over a period of three years. Altogether 3397 patients were investigated. On classification of the patients according to the number of shock indicators, two comparable groups (B and C) of "mild" infarction with 0, 1 or 2 signs of shock were obtained. These low-risk groups comprised 728 patients. The mortality in group C ("mild" infarction, no streptokinase) was 17.3%, significantly higher (p less than 0.01) than the corresponding figure of 10.5% in group B ("mild" infarct, streptokinase therapy). The decrease in mortality by streptokinase therapy applied both to monitored patients as well as to those who were not monitored. Haemorrhage was a very rare complication, but somewhat more frequent in the streptokinase-treated cases, as expected. The incidence of complications such as stereocardia, asystole, and cardiac insufficiency, as well as the conversion of "mild" cases into a "severe" symptomatology was markedly reduced in the streptokinase-treated group.
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PMID:[Results of the Austrian myocardial infarction study on the effects of streptokinase (author's transl)]. 33 53

Lignocaine is widely used as a local anaesthetic and antiarrhythmic drug. It is commonly administered to patients with acute myocardial infarction as prophylaxis for ventricular fibrillation, although its efficacy in preventing primary ventricular fibrillation is still debated. Toxicity, sometimes with serious clinical consequence, is not uncommom and is usually related to overdosage. Blood lignocaine concentrations correlate roughly with antiarrhythmic and toxic effects and might be useful as an end point for monitoring prophylactic therapy. Administration of lignocaine as a local anaesthetic may result in blood lignocaine concentration in the antiarrhythmic or even toxic ranges. Expected peak levels for various routes of local anaesthesia are tabulated so that 'safe' total doses can be calculated. Intramuscular injection of high doses results in sustained therapeutic levels but is often associated with early minor toxicity. Lignocaine is eliminated primarily by hepatic metabolism, which appears to be limited by liver perfusion. Active metabolites may contribute to therapeutic and/or toxic effects. Disease states such as cardiac failure or drugs that alter hepatic blood flow may significantly affect lignocaine clearance. Pharmacokinetic studies in man show wide variability in drug disposition between patients, even when cardiac and hepatic status is considered, making specific dosing recommendations a problem. With intravenous injection, multicompartment kinetics is observed, with an initial rapid decline phase and initial decline in antiarrhythmic activity due to redistribution. With constant infusion, steady state concentrations of lignocaine are seen after 3 to 4 hours in normal subjects and after 8 to 10 hours in patients with myocardial infarction without circulatory insufficiency. In patients with cardiac failure, blood lignocaine concentration may continue to rise for 24 to 48 hours. In the presence of cardiac failure, decreased volumes of distribution and clearance require reduction in loading and maintenance doses. Lignocaine clearance is reduced in patients with liver disease and appears to be a sensitive index of liver dysfunction. A dosing algorithm for treatment of patients with myocardial infarction is presented.
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PMID:Clinical pharmacokinetics of lignocaine. 35 Apr 70

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 method of radionuclide cardangiography (RNCA) has become a well-established method amongst non-invasive assessments in coronary heart disease (CHD). By means of RNCA the most important parameters of left ventricular function, viz. ejection fraction (EF) and wall motion (WM), can be determined very exactly. The first bolus pass method (FBP), which allows satisfactory separation between right and left heart, enables the additional determination of EF distribution, stroke volume (SV) and SV distribution. This method requires the technical necessity of a multicrystal gamma camera. Special nuclear medicine characteristics have been worked out for different groups of CHD. EF and WM show typical signs of angina pectoris, caused by exercise correlating with reduced perfusion in the referring section of WM. While these changes may be reversible after nitrate administration, pathological myocardial function caused by acute myocardial infarction (AMI) or manifest heart failure is not reversed by nitroglycerine. Typical findings were seen in the course of AMI: initial decrease in global EF and diffuse (multilocated) asynergies in the left ventricular wall; in the second week possible start of recovery, including regression of dyskinesia to akinesia at the end of hospitalization. Especially in the early phase of AMI it was demonstrated that FBP--as a non-invasive technique--gives high information quality which is unequalled by other comparable methods. Therefore, the described method of FBP should be classified as very useful and effective in clinical cardiology.
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PMID:[Radionuclide cardangiography as non-invasive assessment in coronary heart disease (author's transl)]. 39 49

Early investigators suggested that ventricular fibrillation without heart failure in acute myocardial infarction was reliably preceded by warning arrhythmias, and that suppression of such arrhythmias with intravenous lidocaine could avoid the need for resuscitation. While the efficacy and safety of lidocaine have been substantiated, the reliability of warning arrhythmias as predictors for primary ventricular fibrillation has not. We present data showing that the risk of primary ventricular fibrillation is most dependent on the patient's age and the interval since the onset of his symptoms, rather than on the presence of warning arrhythmias. We have estimated that lidocaine prophylaxis would have to be given to about 12 patients in the highest risk group (patients under age 50 and within six hours of the onset of symptoms), compared to about 400 patients in the lowest risk group (patients above age 70 and more than 24 hours since the onset of symptoms), to prevent one episode of primary ventricular fibrillation in each group. We propose that these risk stratifications, as adapted to the conditions in specific hospitals, provide the most rational approach to lidocaine prophylaxis of primary ventricular fibrillation.
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PMID:Risk-benefit stratification as a guide to lidocaine prophylaxis of primary ventricular fibrillation in acute myocardial infarction: an analytic review. 39 60

Treatment by phentolamine was carried out in 30 patients presenting with an acute myocardial infarction complicated by left ventricular failure, 8 of which had cardiogenic shock. The response to treatment was closely related to the level of overload of the left ventricle. Significant improvement in the haemodynamic state was only observed in the most severe cases of cardiac failure, and in these cases was accompanied by only a minimal and insignificant change in mean arterial pressure and heart rate.
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PMID:[Vasodilator treatment of the acute phase of myocardial infarct with phentolamine. Analysis of hemodynamic results and therapeutic indications]. 41 75

In 850 patients with acute myocardial infarction, cardiac output has been checked daily with acid-base-balance determinations, respiratory alcalosis being a sign of decreased cardiac output. In 84 patients without spontaneous increase of low cardiac output, treatment with cardiac glycosides has been started with the aim to prevent delayed cardiogenic shock: only 1 patient died in delayed cardiogenic shock and 3 patients in delayed heart failure. In the remaining 766 patients, only 1 patient died in delayed heart failure. With this successful prevention, the overall hospital lethality has dropped to 11.06% as compared with 21.70% in 3272 comparable patients in the literature.
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PMID:[Prevention of delayed cardiogenic shock in 850 patients with myocardial infarction (author's transl)]. 41 6


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