Increased plasma cyclic guanosine monophosphate concentration in chronic obstructive pulmonary disease patients with increased circulating atrial natriuretic peptide.
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Biomedical subjects
Publications and source records attributed to J Labrousse.
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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.
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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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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.