[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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In a group of 14 patients (7 males and 7 females) ventilated artificially for acute respiratory distress syndrome, the authors defined a level of optimal expiratory positive pressure giving an FiO2 = 1, an arterial pO2 greater than or equal to 400 mmhg and/or an intrapulmonary shunt less than or equal to 15%. Improvement in arterial pO2 under such conditions would appear to be related to maximum alveolar recrutment. This optimal level of expiratory positive pressure would appear to be independent of values of total static pulmonary compliance. The long term use of this technique would seem to be encouraging.
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To determine the influence of intermittent positive pressure breathing (IPPB), the level of pulmonary capillary wedge pressure (PCWP) was compared during IPPB and after a short period off the respirator in 68 occasions on 42 patients with an acute respiratory failure (ARF) of various etiologies. During IPPB, the average PCWP was in the normal range in patients with toxic or neurologic comas and in cases of increased pulmonary capillary permeability edema (IPCPE), PCWP slightly increased within chronic obstructive pulmonary disease (COPD) complicated with ARF and in hemodynamic acute pulmonary edema (HAPE). During the weaning stage, PCWP decreased in the groups of coma, COPD, and IPCPE, but increased in HAPE. The weaning test demonstrates that IPPB influenced PCWP in all patients. Therefore, PCWP cannot be assumed to represent the left ventricle filling pressure. The weaning test allows differentiation of IPCPE from HAPE. In the event of over-infusion or hypovolemia, PCWP measured under IPPB can lead to misinterpretation if not followed up by a second measurement off the respirator.
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