Mechanical and non-mechanical ventilation of respiratory failure in chronic obstructive pulmonary disease.

Among 182 episodes with ARF (PaCO2 > 50 torr) in 400 episodes of COPD patients who were admitted to Chulalongkorn Hospital during the period 1982 to 1986, despite conservative treatment, 66 developed severe acute respiratory failure requiring assisted ventilation. Patients with a history of chronic cough, pneumonia as a precipitating factor and more severe ARF on admission, as indicated by palpitation, headache, cyanosis, alteration of consciousness, cor-pulmonale and decompensated acidosis (pH < 7.30), were likely to require mechanical ventilation. Indications for mechanical ventilation were carbon dioxide narcosis (43 episodes), severe hypoxemia despite on a high FIO2 (one episode), various combination parameters of respiratory muscle fatigue, cardiovascular instability (22 episodes). The major complications of mechanical ventilation were pneumonia, sepsis, pneumothorax, UGI bleeding of 16, 8, 5 and 9 episodes, respectively. The average duration of assisted ventilation and hospitalization were 15.8 and 19.02 days, respectively. The mortality rate was 50 per cent in the mechanical ventilation group compared with 9.8 per cent in the non-mechanical ventilation group. Increased mortality rate was found in those with pneumonia as the precipitating factor (68.4 vs 14.3%, respectively, in comparing the two groups). Complications of mechanical ventilation, which included pneumonia, sepsis, fluid overload, hyponatremia and persistent acidosis, were high-risk factors for the non-surviving group.

Amikacin pharmacokinetics in plasma and pleural fluid.

The pharmacokinetics of amikacin in plasma and pleural fluid were studied in nine adult patients with pleural effusions. After a single intravenous bolus of 7.5 mg of amikacin per kg, concentrations in plasma and pleural fluid were measured by fluorescence polarization immunoassays. Pleural fluid pH and PCO2 were also measured. The plasma pharmacokinetics was similar to other studies. However, in the present study the central compartment was significantly greater than the peripheral compartment. Our study suggested that there might be a significant binding of amikacin to the inflamed and/or damaged pleural as suggested by the significant correlations between the apparent volumes of distributions of central and total compartments with pleural fluid pH and PCO2. In pleural fluid, amikacin kinetics followed a large reservoir model with maximum concentration, 4.34 +/- 0.50 mg/L, occurring at 5.64 +/- 0.67 hours post-dose and its half-life was 13.50 +/- 2.93 hours. This concentration was lower than the minimal inhibitory concentration (MIC) for most of the sensitive strains of Gram-negative bacilli and therefore the antibiotics should be given as early as possible for gram-negative pneumonia.