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Biomedical subjects

J F Enrico

Publications and source records attributed to J F Enrico.

At least 19 recordsLinked to original sources
PubMed1989

[Arrhythmogenic ventricular dysplasia or Uhl's disease?].

Uhl's anomaly and arrhythmogenic right ventricular dysplasia are characterized by an analogous morphologic lesion which can be attributed to a major or minor expression of the same genetic disorder. The clinical diagnosis of arrhythmogenic dysplasia is not always easily established. A 23-year-old patient is discussed who showed extrasystolic arrhythmia, electrocardiographic signs of myocardial impairment and syncopes, the latter proving fatal. The segmental absence of myocardial tissue in the right ventricle is associated with interstitial sclerosis of the left ventricular myocardium. Subsisting myocardial fibers might be at the origin of a conduction slowdown creating an intraventricular reentry mechanism. The diagnosis should be considered in young subjects, more frequently males, with some years' history of palpitations, malaise with or without syncopes, and nonspecific electrocardiographic signs such as retarded activation of right cavities (S wave in derivations I and V6, possible right bundle block) and, during ventricular tachycardia, signs of delayed activation of left chambers, a right axis or an extreme deviation to the left.

Adult↗
PubMed1989

[Prevention of recurrence of thromboembolic disease: maintenance of anticoagulant therapy].

Deep venous thrombosis and pulmonary embolism are frequently diagnosed in patients encountered in a primary-care practice. Poor prognosis is related to acute sudden death and to recurrent thromboembolic disease. Anticoagulant therapy with heparin followed by coumarin derivatives is highly effective in preventing such recurrences, but the intensity of anticoagulation must be strictly monitored. Treatment with heparin, sufficient to prolong the activated partial prothrombin time to 1.5 to 2.0 times the control, should be continued for five to ten days, and oral anticoagulation should be overlapped with heparin for four to five days. The recommended therapeutic range for the prothrombin time during coumarin therapy is an INR of 2.0 to 3.0. The duration of anticoagulant treatment must be tailored to the individual patient. Patients with slowly resolving risk factors must be treated for at least three months after an acute deep vein thrombosis and for six months after a pulmonary embolism. Patients with tumors, antithrombin III, protein C or S deficiency should be treated indefinitely.

Anticoagulants↗
PubMed1988

[Activities of intensive care units in 1986].

Based on a yearly evaluation carried out by the Swiss Society for Intensive Care Medicine and the Swiss Nurses Association, statistical reports for 1986 from 72 recognized intensive care units are presented.

Critical Care↗
PubMed1984

Pharmacokinetics of tenoxicam in healthy human volunteers.

Tenoxicam, a thieno-thiazine derivative, belongs to a new chemical class of non-steroidal anti-inflammatory drugs. Single dose kinetics was investigated after intravenous and oral administration to define the disposition and general absorption characteristics of the drug. After intravenous administration of 20 mg tenoxicam to 12 volunteers the time course of the plasma concentrations of unchanged drug followed two-compartment model characteristics. The area under the plasma-concentration time curve in the distribution phase contributed however only 3% or less to the total area. The plasma clearance was low with values ranging from 1.3 to 4.2 ml/min and the volume of distribution Vss was small averaging at 20 to 40% of the total body weight. The median half-life of elimination from the body was found to be 72 hours (range 42 to 100 hours). The disposition was not influenced by sex. Tenoxicam is highly bound to plasma albumin. At pH 7.4 the fraction bound exceeded 99% but was highly dependent on the pH. Plasma protein binding in patients with rheumatic disease was not different from that measured in healthy volunteers. The partitioning of tenoxicam into red blood cells was limited. Erythrocyte concentrations were only 20-30% of the corresponding plasma concentrations. After oral administration of a 20-mg tablet complete and rapid absorption of the drug was observed with maximum plasma levels of 1.7 to 3.6 micrograms/ml reached within 0.5 to 2 hours. Due to the rapid absorption and terminal half-life of the drug its plasma concentration profile after oral administration was very similar to that following intravenous dosing. The pharmacokinetic characteristics of tenoxicam offers a rationale to administer the entire dose in one single portion.

Administration, Oral↗
PubMed1980

[Therapy of ventricular tachyarrhythmia with disopyramid phosphate].

A controlled multicenter study has been carried out in 46 patients with ventricular tachyarrhythmias to define the antiarrhythmic effect of disopyramide phosphate. Monitoring of cardiac rhythm was performed during the whole study period by ambulatory Holter recording. The daily dose of disopyramide was 600 mg. It was found that disopyramide caused a reduction of at least 80% in the number of premature ventricular beats in 72% of the patients. Episodes of ventricular tachycardia were effectively suppressed in 65% of the patients. In 24 patients there was a reduction in the severity of the observed ventricular arrhythmias of at least one class in the classification of Lown. Analysis of the results showed a relationship between the antiarrhythmic effect and group mean plasma concentration of disopyramide.

Adult↗
PubMed1979

[Various aspects of respiratory emergencies in non-hospital practice].

Classical symptoms and signs common to most pulmonary diseases, such as dyspnea, cough, chest pain and cyanosis, are reviewed to assess their significance for diagnosis and evaluation of the degree of impairment in acute respiratory failure. While frequently useful for diagnosis, they are often inadequate to determine the degree of emergency. In each particular etiology other information is needed to obtain an objective and quantitative assessment. Two examples selected for their frequency are considered: barbiturate intoxication and severe exacerbations of asthma. The severity of barbiturate poisoning can be assessed clinically in the light of the degree of central nervous depression. Classical signs and wheezing are poorly correlated with the intensity of acute asthmatic attacks, but high-risk patients can be identified by seeking neglected physical findings such as pulsus paradoxus and sternomastoid muscle contraction. In many other pulmonary emergencies further studies are required to assess the usefulness of various clinical signs as objective indices of the severity of respiratory impairment.

Adult↗
PubMed1976

[The value of alkalizing treatments in severe diabetic keto-acidosis].

In 37 diabetic patients with severe acidosis (pH less than 7.0; [HCO3-] less than 5.0 mMol/l), administration of insulin was preceded by a rapid infusion of molar sodium bicarbonate in order to obtain partial correction of acidosis (pH approximately 7.20). 31 patients survived (83,8%); 6 patients died in cardio-circulatory failure associated in two cases with acute pulmonary edema. Initial administration of bicarbonate appears to be beneficial in preventing the deleterious effects of prolonged severe acidosis, such as cardiac arrhythmias, shock or acute pulmonary edema. Furthermore, partial correction of acidosis decreases the total dose of insulin necessary to compensate hyperglycemia and thereby reduces the danger of late hypoglycemia. This treatment calls for frequent checks on acid-base status and serum potassium. In most cases hypokalemia develops, but can be easily corrected by administration of potassium chloride. Normalization of arterial pH by bicarbonate infusion is not recommended in view of the development of late hypernatremia and metabolic alkalosis.

Acid-Base Equilibrium↗
PubMed1975

Haemodynamic response to slow plasma volume expansion in uncomplicated myocardial infarction.

Left ventricular performance in 16 patients with uncomplicated acute myocardial infarction (AMI) has been estimated, by measuring the haemodynamic response to a moderate increase in left ventricular filling pressure (LVFP), obtained by an espansion in blood volume with a slow infusion of 250 ml of plasma. In 9 cases the infusion was repeated. This represents a total of 25 tests. In 17 tests (group A) cardiac index (CI) and left ventricular stroke work index (LVSWI) did not increase significantly and sometimes decreased. In 8 tests (group B) The same plasma volume expansion (PVE) induced a moderate but significant increase in CI(p less than 0.001) and LVSWI (p less than 0.001). A higher incidence of inferior wall infarction was present in group B. Control CI and LVFP did not differ between the two groups and there was no correlation between the initial LVFP and the type of response to PVE. For the same volume load, the increase in pulmonary capillary wedge pressure (CWP) showed large individual variations (+1 to +8 mm Hg). As a general rule when CI improved, the increment in CWP was minimal (+1 mm Hg). It is concluded that there is no unique optimal LVFP and that PVE must be carefully monitored, in all cases.

Adult↗
PubMed1975

Phentolamine for vasodilator therapy in left ventricular failure complicating acute myocardial infarction. Haemodynamic study.

In 15 patients with acute myocardial infarction associated with signs of left ventricular dysfunction, phentolamine was infused intravenously in a dose of 10 mg per hour. This therapy induced a substantial reduction in mean right atrial pressure from 10 to 7 mmHg (1.3 to 0.9 kPa) (P) less than 0.001), and in pulmonary capillary wedge pressure from 20 to 13 mmHg (2.7 to 1.7 kPa) (P less than 0.001). The cardiac index increased from 2.5 to 3.0 1/min per m-minus 2 (P less than 0.001) accompanied by a fall in both the systemic and pulmonary vascular resistances (P less than 0.001). On the other hand, the mean stroke work index did not change significantly after phentolamine, because of tar resistance. With the dose used the mean arterial pressure decreased from 112 to 99 mmHg (14.9 to 13.2 kPa) (P less than 0.001). No adverse effects attributable to the drug treatment were noted. Benefits of this treatment are probably related to reduction in the impedance of left ventricular ejection and possibly to its relaxant effect on the venous tone. The drug may also improve subendocardial perfusion by decreasing left diastolic ventricular pressure. This could possibly limit extension of necrosis. Thus vasodilator therapy appears to be of particular interest in left ventricular failure complicating acute myocardial infarction, where inotropic agents may be contraindicated.

Adult↗