Chronic obstructive pulmonary disease (COPD) is a common problem in the elderly. The disease is characterised by intermittent worsening of symptoms and these episodes are called acute exacerbations. The best estimate, based on several lines of evidence, is that approximately half of all exacerbations are caused by bacteria. These lines of evidence include studies of lower respiratory tract bacteriology during exacerbations, correlation of airways’ inflammation with results of sputum cultures during exacerbations, analysis of immune responses to bacterial pathogens, and the observation in randomised, prospective, placebo-controlled trials that antibacterial therapy is of benefit. The most important bacterial causes of exacerbations of COPD are nontypeable Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae and Chlamydia pneumoniae.

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Chronic obstructive pulmonary disease

THE respiratory system consists essentially of two parts: a gas-exchanging organ — the lungs—and a pump that ventilates the lungs. The pump consists of the chest wall, the respiratory muscles that ...

The respiratory muscles.

The effects of the administration of 100% oxygen on minute ventilation (VE) and arterial blood gases were studied in patients with chronic obstructive pulmonary disease during acute respiratory failure. The administration of O2 resulted in an early decrease in VE, which averaged 18% +/- 2 SE of the control VE, and was due to a decrease in both tidal volume (VT) and respiratory frequency (f). This was followed by a slow increase in VE, such that after 15 min of breathing O2, VE rose to 93 +/- 6% of the control room air value, with both VT and f similar to control values. Despite the small difference between VE while breathing room air and that at the fifteenth minute of O2 inhalation, PaCO2 increased by 23 +/- 5 mmHg, and no significant correlation was found between the changes in VE and PaCO2. By the fifteenth minute of O2 inhalation the PaO2 averaged 225 +/- 23 mmHg, and it was concluded that despite the removal of the hypoxic stimulus of O2 inhalation, the activity of the respiratory muscles remained great enough to maintain VE at nearly the same degree as that while breathing room air. Consequently, the changes in PaCO2 after the administration of O2 were mainly due to increased inhomogeneity of VA/Q distribution within the lungs.

Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure.

We prospectively examined the pattern of breathing in patients being weaned from mechanical ventilation: one group (n = 10) underwent a successful weaning trial and were extubated, whereas another group (n = 7) developed respiratory failure and required the reinstitution of mechanical ventilation. During the period of ventilator support, minute ventilation (VI), tidal volume (VT), and respiratory frequency (f) were similar in the 2 groups. After discontinuation of the ventilator, VI remained similar in the 2 groups, but VT was lower and f was higher in the patients who failed the trial compared with those who were successful, 194 +/- 23 and 398 +/- 56 ml (p less than 0.001), respectively, and 32.3 +/- 2.3 and 20.9 +/- 2.8 breaths/min (p less than 0.001), respectively. The failure group displayed a significant increase in PaCO2 (p less than 0.005) during spontaneous breathing, without a concomitant increase in the alveolar-arterial PO2 difference. Eighty-one percent of the variance in PaCO2 was accounted for by the pattern of rapid, shallow breathing. During weaning, resting respiratory drive (reflected by mean inspiratory flow, VT/TI) and fractional inspiratory time (TI/Ttot) were similar in the 2 groups. The patients in the failure group showed significant increases in VT/TI, 265 +/- 27 to 328 +/- 32 ml/s (p less than 0.01), and VI, 5.82 +/- 0.53 to 7.32 +/- 0.52 L/min (p less than 0.01), from the beginning to the end of the weaning trial; VT and f showed no further change.(ABSTRACT TRUNCATED AT 250 WORDS)

The pattern of breathing during successful and unsuccessful trials of weaning from mechanical ventilation.

Breathing Patterns: 2. Diseased Subjects

Summary 1. Using the mouth occlusion pressure tech­ nique, we have studied the control of breathing in seven hypercapnic and eight non-hypercapnic patients with chronic obstructive lung disease. 2. When breathing room air, pulmonary ven­ tilation, mean inspiratory flow and P0.i (mouth occlusion pressure developed 0-1 s after the onset of occluded inspiration at functional residual capacity) were not significantly different between the two groups of patients. Tidal volume, however, was significantly lower in the hypercapnic than in the non-hypercapnic patients, as a result of a significantly lower duration of inspiration. 3. The lower tidal volume in the hypercapnic patients leads to decreased alveolar ventilation, and appears to be the main cause of retention of carbon dioxide.

A. Grassino

Papers

Control of breathing in patients with chronic obstructive lung disease.