Effects of diuresis on the characteristics of pleural fluid in patients with congestive heart failure.

PURPOSE: The pleural fluid that accumulates secondary to congestive heart failure is almost always a transudate based upon its level of protein and lactic acid dehydrogenase (LDH). Previous work has suggested that the characteristics of the fluid may change into those of an exudate with diuresis. The purpose of the present study was to determine whether aggressive diuresis does result in this change in pleural fluid characteristics. PATIENTS AND METHODS: Twelve patients with severe congestive heart failure (ejection fraction 23.9 +/- 9.6%) and pleural effusions were studied serially as they underwent diuresis. After an initial thoracentesis was performed, the patients then underwent aggressive diuresis for 12 to 48 hours with one or two follow-up thoracentesis. RESULTS: The mean weight loss during the study period was 4.5 +/- 2.8 kg. With diuresis the LDH level, LDH ratio, protein level, and protein ratio all increased significantly (p less than 0.05). All 12 patients had transudative pleural effusions at the onset of diuresis. However, despite the increases in the levels of protein and LDH with diuresis, only one patient's pleural fluid attained values compatible with an exudate. CONCLUSION: From this study we conclude that it is uncommon for a transudative pleural effusion due to congestive heart failure to develop the characteristics of an exudative pleural effusion with rapid diuresis.

Nebulizer vs spacer for bronchodilator delivery in patients hospitalized for acute exacerbations of COPD.

This double-blind crossover study compared the efficacy of two methods of delivery (MDI-spacer and nebulizer) of inhaled albuterol to patients hospitalized for an acute exacerbation of COPD. Within 24 h of admission, 20 subjects (mean age, 69 years) with severe airflow obstruction (mean FEV, 0.69 L) were subjected to a treatment with an MDI-spacer (0.36 mg of albuterol or placebo) followed by treatment with a nebulizer (2.5 mg of albuterol or placebo). Active drug was given by only one device (randomly assigned in a double-blind manner), and the entire sequence was repeated in 4 h, with active drug given in the alternate device. Spirometric data and the Borg dyspnea score were obtained before and 1 h after each sequence of treatments. Treatment resulted in significant improvements in the FEV1, FVC, and Borg score. The percent improvement in the FEV1 was slightly larger after treatment with the nebulizer (16.7 percent vs 13.4 percent). Improvements in the Borg score were slightly larger after treatment with the MDI-spacer (-1.08 vs -0.73). However, these differences were not statistically significant. This study suggests that the MDI-spacer system is an effective method of sympathomimetic delivery in this setting, provided patients are able to master the technique.

Cardiopulmonary responses to exercise in chronic airflow obstruction. Effects of inhaled atropine sulfate.

The purpose of this study was to evaluate the effects of inhaled atropine sulfate on the exercise capacity and cardiopulmonary responses to exercise in patients with chronic airflow obstruction (CAO). Eighteen patients underwent duplicate incremental (15 watts/min) maximal cycle ergometer exercise tests 60 minutes after either inhaled atropine (0.075 mg/kg) or placebo, in double blind randomized fashion on consecutive days. Bronchodilator medications were withheld before each study. Spirograms were obtained before and 60 minutes after each aerosol treatment. Atropine increased the FEV1 by 25 percent, from 1.37 +/- 0.49 to 1.71 +/- 0.52 L (p less than 0.001), as compared to placebo. Although the ventilation at exhaustion (VEmax) increased significantly (from 52.3 +/- 11.5 to 55.9 +/- 10.0 L/min, P less than 0.05) after atropine, the increase in the mean maximum work load (95 +/- 28 vs 101 +/- 19 watts) did not achieve significance. The drug resulted in a significant decrease in oxygen consumption at all equivalent workloads greater than "0" watts (unloaded cycling), presumably because the improvement in airway mechanics decreased the oxygen cost of ventilation. Atropine-induced increases in FEV1 did not result in a significant group mean increase in maximum exercise capacity, but the drug did result in a lower oxygen cost of performing work in patients with CAO.

Effect of inhalate thermal conductivity and high O2 in producing hypothermia.

The effect of an increase in inhalate thermal conductivity and the fraction of inspiratory O2 (FIO2) on the rate of cooling and rewarming using a surface-inhalate heat exchange method was evaluated. Male New Zealand White rabbits were divided into three groups: those ventilated with air, those with 20% O2 + 80% He, and those with 100% O2. All animals were cooled to an esophageal temperature of 22.5 degrees C (or for 180 min maximum). Following a 15-min exposure to room air, the animals were connected to the humidifying and warming system. He-O2 had the highest thermal conductivity and the animals ventilated with it had the fastest cooling rate. One hundred percent O2 and room air had similar thermal conductivities, but the animals ventilated with 100% O2 had significantly lower cooling rates. These data indicate that, while maintaining a constant surface heart exchange, the rate of heat exchange across the lung can be modified by altering the thermal conductivity of the inhalate gas mixture. Total heat exchange can also be modified by hyperoxemia-induced hemodynamic changes.

Effect of hypothermic anoxic cardioplegia on myocardial contractility.

A study was undertaken to ascertain the protective effect of topical hypothermia on the anoxic heart. The presence or absence of myocardial damage was judged by myocardial contractility. The papillary muscle of an excised rabbit heart was detached from the mitral annulus and interposed between a fixed point and a force/displacement transducer. The maximal net developed tension (TNmax) of the papillary muscle with normothermic coronary perfusion was used as an index of myocardial contractility. With each temperature drop of 10 degrees C, the anoxia time that resulted in the same recovery level of TNmax was prolonged by a factor of 2.8. A nomogram was constructed correlating percent of myocardial recovery seen with different degrees of myocardial hypothermia during various anoxic periods. Optimum protection was noted at a myocardial temperature of 18 degrees C.