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

The diagnosis of lactate acidosis is complicated by the fact that lactate determination is not a routine method in clinical chemistry. In fact, lactate analysis is performed only in special laboratories. Even in greater clinics this method is not routinely performed in differential diagnosis of acidotic states. Various diseases are accompanied by a lactate emia or even by lactate acidosis. Anaerobic synthesis of lactate is an emergency reaction to supply minimum energy to tissues with insufficient oxygen supply. The main diseases complicated by increased blood lactate concentrations are shock, circulatory collapse, cardiac failure and peripheral circularoty disturbance. Additionally diabetes mellitus, septical infections, and-the most prominent situation-biguanide intoxications are complicated by an increase in blood lactate concentration.
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PMID:[Clinical picture of lactate acidosis. 4: Clinical significance of lactate acidosis]. 2 Mar 98

Blood loss of sufficient magnitude to over-ride compensatory mechanisms and result in a lowering of arterial pressure will ultimately lead to irreversible circulatory collapse. Identification of the organ or tissues which may trigger a terminal cascade remains controversial. The weight of evidence supports the view that cardiac performance deteriorates with prolonged oligemic hypotension, although this may not be the initiating or sole reason for irreversible failure of the circulation. Controversy regarding the heart as an important target organ is no doubt in part due to the multiplicity of preparations and protocols, and variety of methods used to characterize cardiac function. We have used ventricular function curves to calibrate LV performance in terms of pump function, while arterial pressure remains at a pre-determined level. With this approach, a progressive decline in stroke volume for a given LV end diastolic pressure is consistently observed in hemorrhagic shock (AP, 30 mmHg). If arterial pressure is briefly re-elevated at 30 minute intervals, permanent deterioration is prevented. However, if the hypotension is sustained for 2 hours, LV performance remains depressed following pressure re-elevation. Among the mechanisms responsible for deterioration of performance, coronary perfusion pressure (CPP) exerts a pivotal role. Thus, no LV depression occurs after 2 hours of shock provided CPP is maintained at normotensive levels. But if myocardial O2 availability falls below 10 ml/min/100 gm of heart, both O2 uptake and extraction decline and this is uniformly accompanied by cardiac failure. This likely reflects mitochondrial damage and impaired aerobic metabolism. These changes are potentiated by the appearance of metabolic acidosis and failure of sympathetic neurohumoral activity. Both factors directly reduce myocardial contractility, but assume much greater importance during shock. While E. coli endotoxin has been shown to reduce cardiac performance, the relative importance of bacterial products which may enter the circulation during hemorrhagic shock in uncertain. Reduced O2 availability, metabolic acidosis and adrenergic failure appear the major determinants of diminished cardiac performance and thereby may contribute to irreversible collapse of circulatory function.
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PMID:Cardiac performance in hemorrhagic shock. 55 6

Following a case of mannitol-induced respiratory and circulatory collapse, the effects of hyperosmolar injections on pulmonary arterial pressure, systemic blood pressure, and cardiac output were studied in dogs. The injection of 20 ml of 10% NaCl into the pulmonary artery increased pulmonary arterial pressure and decreased systemic blood pressure by approximately 50% of control values. Injections of solutions of equal hyperosmolar strength, 50 ml of 25% mannitol or 50 ml of 4% NaCl into the pulmonary artery produced no significant elevation of pulmonary arterial pressure, but were associated with comparable decreases in systemic blood pressure. When allowed to vary, cardiac output increased with injections of all three hyperosmolar solutions, yet was still accompanied by falls in systemic blood pressure as large as when cardiac output was held constant. Vagotomy did not prevent these changes in systemic and pulmonary arterial pressure, nor the increase in cardiac output. After five to 10 injections, the decreases in system blood pressure with any of the solutions and the increases in pulmonary arterial pressure with 10% NaCl disappeared and further injections were without effect. It is concluded that adminstration of mannitol probably does not cause pulmonary edema due to fluid overload, nor does it cause heart failure as evidenced by increases in pulmonary arterial pressure. However, rapid injection may cause a fall in blood pressure and may on occasion be accompanied by bronchospasm, especially in sensitive subjects.
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PMID:Hypotension and respiratory distress caused by rapid infusion of mannitol or hypertonic saline. 57 Dec 22

The effects of amiodarone by injection have been studied in 100 patients. 50% of these patients were in cardiac failure. Amiodarone was given intravenously over 30 seconds in a dose of 300 mg; in 15 of the patients a further dose of 150 mg was given after ten minutes. Amiodarone was found to be particularly effective in the tachy-arrhythmias (90% successful) in which it brought about slowing (18 cases out of 30) or conversion (17 cases out of 30). Just as good results were obtained for the atrial tachycardias (90% success rate) and in the junctional tachycardias. This treatment is less effective for atrial flutter (50% successful) and for ventricular arrhyrthmia, in which the success rate was only 60%. It is possible to use the defibrillator after amiodarone has been administered. This drug is well tolerated, and no increase in cardiac failure has been noted in these patients. There does remain, however, the possibility of hypotension and perhaps of circulatory collapse, which is rapidly reversable; this is probably due to vasodilator activity. Intracavitary studies in 8 patients have shown that amiodarone causes slowing of sino-atrial and of atrio-ventricular conduction. Amiodarone may equally worsen a distal conduction defect. The uses for this anti-arrhythmic drug, which is particularly effective at the atrial level, are discussed in this paper.
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PMID:[Anti-arrhythmic effects of injectable amiodarone. Apropos of 100 cases]. 82 21

Hemorrhagic atelectasis was successfully produced in newborn rabbits by pharmacologically narrowing airways leading to alveoli ventilated with oxygen-enriched gas. Between 48% and 62% of alveoli filled with blood cells. Areas of lung with a tendency to collapse were measured by pressure volume studies. Animals given supplemental oxygen retained 56% of total lung volume compared with 79% in the pilocarpine group, which suggested increased effectiveness of anti-atelectasis factors in the latter. Less total lung gas was present in the pilocarpine group (4.0 plus or minus 0.4 cc/g) compared with oxygen controls (5.1 plus or minus 0.81 cc/g), which indicated more noninflatable lung. Neither surfactant deficiency nor heart failure needed to be present for pulmonary hemorrhage to occur.
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PMID:A new model for neonatal pulmonary hemorrhage research. 117 May 42

In 56 patients, frequency analysis of the electrocardiogram of ventricular fibrillation exhibited power spectra with a distinct dominant frequency. The greatest success for resuscitation from ventricular fibrillation is recorded when ventricular fibrillation develops after the patient comes under coronary care. Of the 41 patients in whom the onset and first 8 s of ventricular fibrillation were artefact-free the mean dominant frequency of primary ventricular fibrillation (no cardiogenic shock or cardiac failure) in 21 patients was 6.2 +/- 0.2 Hz, significantly higher than the mean dominant frequency of the first 8 s of secondary ventricular fibrillation (cardiogenic shock or heart failure) (4.0 +/- 0.2 Hz, 20 patients, p = 0.0001). In these patients the peak-to-trough amplitude (ECG) of the first 8 s of ventricular fibrillation was similar in both primary and secondary ventricular fibrillation as was the mean duration of ventricular fibrillation prior to the first DC shock. There was a significantly lower success rate for resuscitation from secondary ventricular fibrillation (6 of 20 patients) compared with resuscitation from primary ventricular fibrillation (18 of 21 patients, chi 2 17.8, p = 0.001). Of the remaining 15 patients who were collapsed between 3 and 20 min before the arrival of the mobile coronary care unit, the dominant frequency of the first 8 s of ventricular fibrillation fell with increased duration of collapse (from 5.5 Hz at 3 min to a mean of 2.1 Hz at 20 min).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Frequency analysis of ventricular fibrillation and resuscitation success. 843 54

Death in normobaric hyperoxia was related in the past to pulmonary insufficiency of the edematous lung. However, high arterial O2 tension on final collapse led to the suggestion that the heart and not the lung is the first organ that fails. We measured aortic flow, coronary flow, left ventricular pressure, affluent and effluent PO2, PCO2, and pH in the working heart excised from control and normobaric O2-exposed rats (51-63 h). The oxygen consumption (VO2) of experimental hearts was not different from control, but mechanical power output (PVAP) (calculated from pressure-volume area) was reduced as a function of O2 exposure time. Myocardial contractility indexes, maximal elastance and maximal time derivative of pressure, increased as a function of O2 exposure time, being below control values after 50 h and above control values after 60 h. The individual slopes for the regression of VO2 vs. PVAP rose as a function of exposure time from values below control after 50 h exposure to values above control after 60 h. Energetic efficiency (PVAP/VO2) decreased as a function of O2 exposure time and points to possible heart failure in the intact animal. After 50 h O2 exposure the heart was energetically more efficient than the control. Possible changes in the heart are discussed.
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PMID:Heart energetic efficiency in O2-exposed rats studied in isolated working heart. 149 Sep 35

Adenosine has recently become widely available for the treatment of paroxysmal supraventricular tachycardia. In order to evaluate its role in the management of arrhythmias, we have reviewed the literature on the cellular mechanisms, metabolism, potential for adverse effects, and clinical experience of the efficacy and safety of intravenous adenosine. Adenosine produces transient atrioventricular nodal block when injected as an intravenous bolus. This is of therapeutic value in the conversion to sinus rhythm of the majority of paroxysmal supraventricular tachycardias, which involve the atrioventricular node in a re-entrant circuit. The mean success rate was 93% from over 600 reported episodes. Compared with other antiarrhythmic agents, adenosine is remarkable for its rapid metabolism and brevity of action, with a half-life of a few seconds. It commonly produces subjective symptoms, particularly chest discomfort, dyspnea, and flushing, which are of short duration only. No serious adverse effect has been reported. Arrhythmias may recur within minutes in a minority of patients. Comparative studies have shown that adenosine is as effective as verapamil in the treatment of supraventricular tachycardia, and has less potential for adverse effects. Patients with supraventricular tachycardia should initially be treated using vagotonic physical maneuvers. Immediate electrical cardioversion is indicated if the arrhythmia is associated with hemodynamic collapse. Adenosine is the preferred drug in those patients in whom verapamil has failed or may cause adverse effects, such as those with heart failure or wide-complex tachycardia. The safety profile of adenosine suggests that it should be the drug of first choice for the treatment of supraventricular tachycardia, but only limited comparative data to support this view are available at present.
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PMID:Adenosine and the treatment of supraventricular tachycardia. 160 47

Thirteen out of 268 children (less than 18 years old) underwent hepatic transplantation (OLT) for end-stage liver disease (ESLD) associated with arteriohepatic dysplasia (AHD). Seven children are alive and well with normal liver function. Six children died, four within 11 days of the operation and the other two at 4 and 10 months after the OLT. Vascular complications with associated septicemia were responsible for the deaths of three children. Two died of heart failure and circulatory collapse, secondary to pulmonary hypertension and congenital heart disease. The remaining patient died of overwhelming sepsis not associated with technical complications. Seven patients had a portoenterostomy or portocholecystostomy early in life; five of these died after the OLT. Severe cardiovascular abnormalities in some of our patients suggest that complete hemodynamic monitoring with invasive studies should be performed in all patients with AHD, especially in cases of documented hypertrophy of the right ventricle. The improved quality of life in our surviving patients confirms the validity of OLT as a treatment of choice in cases of ESLD due to AHD.
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PMID:Liver transplantation for arteriohepatic dysplasia (Alagille's syndrome). 162 41

A case is reported of a 50-year-old man who took a massive overdose of diltiazem (5,400 mg), together with 1,350 mg potassium clorazepate and 390 mg nordazepate, five months after having experienced a myocardial infarction (MI). On admission, systolic blood pressure was 80 mmHg, with an irregular heart rate of 60 b.min-1. There was superficial polypnea (40 c.min-1) with hypoxia (PaO2: 63.5 mmHg). The ECG revealed, besides the MI scar, complete sinus arrest. Endotracheal intubation and mechanical ventilation were rapidly required. The patient then had gastric lavage, and was given activated charcoal. Treatment with 1.5 mg atropine and 2 g intravenous calcium chloride were unable to amend the cardiac dysrhythmia. A continuous isoproterenol infusion restored a sinus rhythm, but this was not maintained because of the risk of side-effects. Cardiovascular collapse was treated with dobutamine (10 micrograms.kg-1.min-1). As the peripheral and pulmonary vascular resistances were greatly diminished (464 dyn.s.cm-5 and 86 dyn.s.cm-5 respectively), alpha and beta mimetics were used: 1 microgram.kg-1.min-1 noradrenaline and 15 micrograms.kg-1.min-1 dobutamine. After 7 h of this treatment, spontaneous sinus rhythm returned abruptly. Noradrenaline and dobutamine were replaced thereafter with adrenaline (0.25 microgram.kg-1.min-1), which was stopped 24 h later. There was a marked respiratory and haemodynamic improvement, the patient leaving the intensive care unit on the fourth day and returning home one week after the overdose. The relationships between cellular calcium movements and the adrenergic system are discussed, as well as the possible mechanism of cardiac failure.
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PMID:[Diltiazem poisoning: hemodynamic aspects]. 167 48


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