[Ancient and current techniques of resuscitation by vascular approach].
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Biomedical subjects
Publications and source records attributed to J Lissac.
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Metabolic alkalosis (MA) only occurs after bicarbonate administration if given quickly and massively, or in the presence of renal failure. Most cases of MA are caused by a loss of hydrogen ions. This paper reviews the common causes (gastric aspiration, chronic diuretic therapy) and updates the list of drugs which may lead to this complication. Rare causes (such as hyper mineralo-corticoid secretion) should be suspected in patients with MA unresponsive to usual doses of potassium chloride. Hydrochloric acid infusions are reserved for very special cases.
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This study examined the relationships between acid-base disorders, hypoxemia, electrolyte imbalances, plasma adrenaline (Ad) and noradrenaline (NAd) in 94 patients with acute severe asthma. Criteria of inclusion were [PaO2 + PaCO2/.8] less than 140 mmHg when breathing air (FiO2 = 21%) and/or PaCO2 greater than or equal to 45 mmHg. PaCO2 was closely related to H+ in those patients with hypercapnia: H+ nmol/l = 0.88 PaCO2 + 4 (r 0.91 ; n = 61; p less than 0.001). However, among the 62 acidotic cases (pH less than or equal to 7.36), 24 were classified as respiratory, 22 as mixed and 16 as metabolic. A loose though highly significant relationship was found between PaO2 and PaCO2 (when breathing air). Blood lactate, which was 3.61 +/- 1.9 mmol/l (+/- SD), was not correlated with anion gap or H+, but was loosely related to PaO2 and kalemia. Ad (1.53 +/- 1.17 nmol/l) and NAd (5.85 +/- 3.44 nmol/l), measured at the time of admission in 27 patients (FIO2 = 21%), varied significantly from those of a control group (p less than 0.01). NAd was correlated with H+, lactate and especially PaCO2, whereas no correlation could be established for Ad with these factors or NAd values. On the average, kalemia, phosphatemia and calcemia were lowered. In conclusion, mixed and metabolic acidosis were more common in this study than in a previous personal series and were not necessarily associated with an increase in blood lactate. Drugs taken prior to hospitalization must be considered in the pathophysiology of hyperlactatemia, which appears to be one among several factors linked to NAd levels.
The aim of this study was to assess the effects of enoximone on the right ventricle and pulmonary hypertension in 10 patients (53 to 84 years) with chronic obstructive airway disease resulting in acute or chronic respiratory failure requiring mechanical ventilation in 9 cases. These effects were compared with those of dobutamine. All patients were in sinus rhythm and 6 had signs of right ventricular failure. Haemodynamic and 2D echocardiographic (study of left and right ventricular function) measurements were made under basal conditions (TB1), with 10 micrograms/kg/mn of dobutamine (TDob), again under basal conditions (TB2) three hours after the end of the dobutamine infusion, and then 30 minutes after an intravenous bolus (1 mg/kg) of enoximone (TE1) relayed by an infusion of 10 micrograms/kg/mn at 3 hours (TE2) and at 12 hours (TE3). The results (x +/- SD) were studied by a 2 factor variance analysis and compared by Student's test with Dunnett's correction. Cardiac index increased similarly by about 45% with enoximone (2.8 +/- 0.8 vs 4.1 +/- 1 l/min/m2; p less than 0.001 at TE2) and dobutamine, although the heart rate did not change significantly. Systemic arterial resistance fell significantly with enoximone (31.3 +/- 11 vs 21.3 +/- 6.8 IU; p less than 0.05 at TE2) but mean arterial pressures were unchanged; mean pulmonary artery pressures decreased from TE1 to TE3 (27.6 +/- 6.9 vs 22.6 +/- 6.3 mmHg; p less than 0.05 at TE2) mainly because pulmonary artery diastolic pressures decreased from TE1 to TE3 (20.1 +/- 4 vs 11.1 +/- 5.2 mmHg; p less than 0.05 at TE3).(ABSTRACT TRUNCATED AT 250 WORDS)
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Although abnormal blood gases are unusual in status asthmaticus, hypercapnia indicates a considerable increase in bronchial resistance. The authors report their experience of 106 personal cases of acute severe asthma. Emergency management of acute respiratory failure consisted in symptomatic therapy (low rate oxygen or mechanical ventilation after nasal intubation). Corticosteroids, rehydration, antibiotics and beta-2 adrenergic agents were associated. Mechanical ventilation was necessary in patients who developed alterations of consciousness or PaCO2 above 60 mm Hg (8 kPa). In respirator-patients, sedative drugs were needed. Terbutaline and salbutamol were occasionally beneficial but epinephrine remains the drug of choice. In our series of 106 cases (79 with hypercapnia) the overall mortality was 3.8 p. 100. Of the 33 cases who underwent mechanical ventilation, there were 4 deaths (12 p. 100). A review of the literature showed a much higher mortality in other series.
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The objectives of this study, in which Almitrine bismesylate was administered for one year in chronic bronchitics with obstructive hypoxia, were to assess its clinical and gasometric efficacy and its clinical, laboratory, spirometric and electrocardiac acceptability. The blood gas results show a significant rise in PaO2 (p less than 0.001) rising by 5.5 mmHg after 6 months (T6) and by 6.0 mmHg after 12 months (T12) in comparison with the value at the study's onset. The PaCO2 fell by 3.3 mmHg at T6 and 2.7 mmHg at T12 (p less than 0.001). The dyspnoea of the patient, scored by the doctor on a scale of severity from 0 to 5 was situated on a mean of 3.3 points at the beginning of the study. It was significantly reduced by 0.8 points at T6 and by 0.9 points at T12 (p less than 0.001). The percentage of patients hospitalised during the course of the study fell significantly in comparison with the previous year, from 68% to 49% (p less than 0.001). The improvement in clinical status and in blood gases bore no relation to changes in respiratory function. The clinical acceptability of the product was good; few side effects were observed and the respiratory, digestive and neurological problems were often pre-existing. They only led to cessation of treatment in three cases. The electrocardiogram was unchanged. The laboratory investigations was unchanged, with the exception of a fall in red blood cells in relation to the correction of the hypoxaemia in polycythaemic patients.
Two cases of interstitial pneumonitis are described which developed after the acute phase of aspiration pneumonitis. Open lung biopsy revealed an interstitial, granulomatous foreign body response induced by foodstuff aspiration. Steroid treatment was administered and both cases then showed a favourable course, with the pulmonary lesion healing within 12 days.
The aim of this study, based on the electrocardiographic analysis of 42 patients in status asthmaticus, is to define the basic criteria which may be used as a basis for electrocardiographic differential diagnosis. The following ECG changes were observed: the pulmonary "p" wave is common, sometimes with exaggerated amplitude in peripheral leads, however, in the precordial leads, the voltage of the "p" wave is reduced; most cases have a vertical heart with clockwise rotation and mild right axis deviation, S1 Q2 Q3 and the transitional zone displaced to the left. Ten cases also had a S1 S2 S3 appearance and three cases showed Q1 Q2 Q3, simulating myocardial infarction; there is poor progression of the R wave in the precordial leads and marked persistence of the S wave in the left precordial leads. In some cases, a QS complex dominates the right precordial leads. A variation in the amplitude of the QRS with the respiratory rhythm is often seen in V1 and V2; ventricular repolarization shows a lowered J point with an upward oblique ST segment in the peripheral leads. However, in the precordial leads, the repolarization is normal except for three cases which presented a frank hypokalaemia. The mechanism of these electrocardiographic changes appears to depend on the vertical position of the heart caused by over expansion of the lungs and pulmonary arterial hypertension. The elements of the electrocardiographic differential diagnosis with myocardial infarction and pulmonary embolism are discussed.
Plasma fibronectin (FNp) concentrations were measured in 63 patients with acute respiratory failure and 28 patients with circulatory failure, using Laurell's electroimmunoassay method. Measurements were made in the acute phase and repeated in the course of the disease. The mean FNp concentration in 20 controls was 262 +/- 59 mg/l. FNp values were normal in the acute phase of chronic obstructive pulmonary disease and in cardiogenic pulmonary oedema. In contrast, they were significantly decreased in adult respiratory distress syndrome and in acute pneumonia, as well as in acute circulatory failure, notably from septic shock. FNp values were also considerably reduced in patients with severe disseminated intravascular coagulation syndrome. Clinical improvement was accompanied by a return to normal of FNp concentrations. The mortality rate was greater in patients with low FNp values than in those with normal values.
Three cases of acute gangrenous acalculous cholecystitis, revealed by a postoperative septic shock, are reported. Clinical examination was negative and the surgery gave the diagnosis. Infection with biliary stasis and ischaemia accounts for this pathological entity. The very serious prognosis of this condition can only be reversed by cholecystectomy.
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This report describes a case of adult respiratory distress syndrome (ARDS) after massive subcutaneous injections of silicone. The patient, a 23 year-old transsexual man, treated with mechanical ventilation, died on the 12th day of hospital, in septic shock and refractory hypoxemia. Autopsy findings revealed empty vacuoles surrounded by macrophages in various organs, especially in lung tissue. Toxicological analysis by emission by high frequency induced plasma showed silicone in the organs with histological lesions. The pathophysiology of this ARDS is considered.