Ventilatory instability in patients with congestive heart failure and nocturnal Cheyne-Stokes breathing.

Many of the factors that appear to cause Cheyne-Stokes Breathing (CSB) in sleeping patients with congestive heart failure (CHF) are present during wakefulness. We studied the stability of ventilatory pattern in nine awake CHF patients (left ventricular ejection fraction 9-48%) who demonstrated CSB only while asleep and compared results with 13 age-matched normals. The test involved brief (30-50-second) exposure to hypoxia (end-tidal PO2 = 55 Torr) followed by breathing pure oxygen. During hypoxia, ventilation increased about 40% above air breathing control in both groups, whereas end-tidal CO2 declined to 92% of control in both groups. During hyperoxia, however, breathing pattern differed between groups. In the normals, ventilation gradually declined to air-breathing levels and did not significantly undershoot. In the patients, ventilation dropped more rapidly to baseline and an overshoot was present with ventilation being 72% and air-breathing control at 45 seconds of hyperoxia. Circulatory delay was calculated from the time interval between alveolar hypoxia and in increase in ventilation, and when corrections for circulatory delay were applied to ventilation during hyperoxia the differences between groups increased in that the patients' ventilation was less than baseline immediately after the delay. In the normals, the gradual decline in hyperoxic ventilation probably represents the decay of short-term potentiation (STP) activated by hypoxic hyperventilation. Results in the patients were compatible with absence of such STP decay, but could also have been due to a reduction in ventilatory drive early in hyperoxia related to prolonged circulation times.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of responses to methacholine and cold air in patients suspected of having asthma.

In 140 adult patients with FEV1 greater than or equal to 60 percent predicted referred because of suspected asthma, we compared responses to methacholine and isocapnic cold-air hyperventilation. Most challenges were accomplished on the same day, cold air always being done first. The cold-air test employed a single episode of hyperventilation (target, 30 times the FEV1), and subsequent FEV1 changes were noted, a decrease of 10 percent being defined as a positive test result. For methacholine, subjects inhaled aerosols of increasing concentrations and the dose associated with a 20 percent decline in FEV1 (PC20) was noted; positive tests were defined as a 20 percent decrease at concentrations less than or equal to 8 mg/ml. Of the 140 patients, 65 had negative results on both challenges. Twelve patients had positive results on cold-air testing but negative responses to methacholine, and 17 had the opposite result. Among patients with positive results to either test, there was a significant correlation (p less than 0.001) between change in FEV1 with cold air and log PC20, but there was considerable scatter, the results of one test accounting for 25 percent of the variability in the other. Some scatter may have been related to the methods we used, but much was probably due to the patients themselves. Neither test should be used on an exclusive basis to make the diagnosis of asthma.

Effect of postoperative intermittent positive pressure breathing on lung function.

Thirty patients undergoing elective cholecystectomy were randomly assigned to two groups. Fifteen patients received postoperative intermittent positive pressure breathing (IPPB) for four days together with physiotherapy while the other 15 had the same postoperative care but without IPPB. Vital capacity (VC), functional residual capacity (FRC) and PO2 were measured preoperatively and on days 0, 1, 3, and 5 postoperatively. The incidence of postoperative pulmonary complications utilizing chest x-ray films, sputum analysis, temperature, and clinical assessment was determined. Both groups had significant deterioration in pulmonary function but did not differ except for a greater depression in VC in the IPPB group (p less than .05). In patients receiving postoperative physiotherapy, the addition of IPPB did not usually result in improved pulmonary function.

The effect of transcutaneous electric nerve stimulation on postoperative pain and pulmonary function.

Surgery on the upper abdomen is associated with marked postoperative pulmonary dysfunction that results largely from restriction of lung expansion secondary to incisional pain. This study, utilizing three groups of patients (a control group, a sham group, and a group receiving transcutaneous electric nerve stimulation [TENS] for pain control), was designed to determine whether this modality is effective in alleviating postoperative pain. Spirometry, arterial blood gases, clinical as well as radiologic evidence of postoperative pulmonary complications, and the frequency of analgesic requests were determined. Of the 40 patients studied, the 15 receiving TENS required only 4.7 +/- 2.5 doses of narcotic analgesics in the first 72 hours as opposed to 10.1 +/- 2.7 and 10.4 +/- 2.7 in the other two groups (P less than 0.005). There were a total of six postoperative pulmonary complications, all occurring in the groups not receiving TENS. Postoperative arterial Po2, vital capacity, and functional residual capacity were least depressed in the TENS group. The data suggest that TENS minimizes the tendency toward postoperative alteration in respiratory mechanics and decreases the incidence of pulmonary complications by alleviating incisional pain.

Respiratory short-term potentiation (after-discharge) in elderly humans.

During a ventilatory stimulus, respiratory short-term potentiation (STP, after-discharge) develops, so that ventilation after the stimulus is greater than that before the stimulus. When the stimulus is withdrawn STP gradually decays, tending to prevent hypoventilation and therefore stabilizing breathing pattern. STP has been demonstrated in young humans after brief hypoxic stimuli. Since respiratory arrhythmias increase with age, we examined the decay of STP in normal elderly humans (mean age 62), comparing them with young normals (mean age 27). Resting subjects were exposed to 35-50 sec hypoxia (end-tidal PO2 = 55 Torr) followed by hyperoxia and breathing analyzed during the hyperoxic period, when the subjects were also hypocapnic. With hypoxia, ventilation increased to 152% of control in both the older and younger subjects while end-tidal CO2 fell to 92.0% of control in the older subjects and 94.7% of control in the younger. In both groups the hypoxic increase in ventilation was almost entirely due to an increase of tidal volume. During hyperoxia, ventilation and tidal volume declined over 20-25 sec to control, pre-hypoxic levels, without an apparent undershoot, and there were no consistent differences between the older and younger subjects. Prolonging the hypoxic exposure to 90 sec had no influence on STP in the older subjects. We conclude that neither age nor prolonging the hypoxic stimulus from 50 to 90 sec influenced STP.

Ventilatory response to hypoxia in elderly humans.

In young adults the ventilatory response to 25 min of isocapnic hypoxia (SaO2 = 80%) is characterized by an initial increase in ventilation followed by a decline. The increase and decline are proportional. Because older adults have been reported to have reduced initial ventilatory responses to hypoxia, we compared responses to hypoxia in 14 older (mean age 62) and 15 younger (mean age 29) subjects. There was no difference. Both groups demonstrated a similar initial increase in ventilation with hypoxia and a similar subsequent decline due to a decline in tidal volume. In both groups the size of the initial increase was proportional to the subsequent decline. In both groups hyperoxia immediately after 25 min of hypoxia transiently depressed ventilation, while hyperoxia after room air breathing did not. We conclude that the ventilatory response to 25 min of hypoxia is independent of age in normal humans.

Response to cold air hyperventilation in normal and in asthmatic children.

To assess the sensitivity of isocapnic hyperventilation with cold air in detecting airway hyperreactivity in asthmatic children, we studied 13 asthmatic patients (mean age 11.1 years) and 10 normal children. Cold air challenge consisted of 4 minutes of moderate hyperventilation plus another 4 minutes of maximal hyperventilation, both with subfreezing air (-16 degrees to -18 degrees C). Exercise and IHCA tests were done within 5 days and in random sequence. Mean (+/- SE) maximal % delta FEV1 after IHCA was 27 +/- 5.1% in the asthmatic children vs 4.5 +/- 1.2% in the normal subjects (P less than 0.01), even though there were no significant differences in the maximal minute ventilation equivalent between the two groups. Mean maximal % delta FEV1 after exercise was 31.7 +/- 5.6 in the asthmatic group. There was no difference in the sensitivity of the exercise and IHCA tests to detect bronchospasm in asthmatic children. Airway obstruction after IHCA was sharp and brief: maximal at 3 minutes after challenge, and back to 10% of baseline after 11 minutes. In seven asthmatic children the refractoriness to cold air and exercise was studied by repeating each test within 30 minutes; all seven showed significant refractoriness to exercise, and six showed no refractoriness to IHCA. We conclude that exercise and cold air-induced bronchospasm have different physiologic mechanisms, and that cold air testing can be used as a routine challenge to identify airway hyperreactivity in children.