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Biomedical subjects

D C Flenley

Publications and source records attributed to D C Flenley.

At least 73 records · Page 4Linked to original sources
PubMed1983

The ventilatory effects of doxapram in normal man.

1. To determine the mode of action of doxapram in man we have measured ventilation, oxygen uptake, CO2 production, hypoxic and hypercapnic ventilatory responses in six healthy men before and during intravenous infusion to maintain a constant plasma level. 2. Doxapram changed neither resting oxygen uptake nor CO2 production but produced a substantial increase in resting ventilation at both levels of end-tidal CO2 studied. 3. Doxapram increased the ventilatory response to isocapnic hypoxia from -0.8 +/- 0.4 litre min-1 (%SaO2)-1 to -1.63 +/- 0.9 litres min-1 (%SaO2)-1. This was similar to the increase in hypoxic sensitivity which resulted from raising the end-tidal CO2 by 0.5 kPa without adding doxapram. 4. The slope of the ventilatory response to rebreathing CO2 rose from 11.6 +/- 5.3 litres min-1 kPa-1 to 20.4 +/- 9.8 litres min-1 kPa-1 during doxapram infusion. 5. The marked increase in the ventilatory response to CO2 implies that doxapram has a central action, but the potentiation of the hypoxic drive also suggests that the drug acts on peripheral chemoreceptors, or upon their central connections, at therapeutic concentrations in normal unanaesthetized subjects.

Adult↗
PubMed1983

Ketotifen and nocturnal asthma.

Patients with asthma often wheeze at night and they also become hypoxic during sleep. To determine whether ketotifen, a drug with sedative properties, is safe for use at night in patients with asthma, we performed a double blind crossover study comparing the effects of a single 1 mg dose of ketotifen and of placebo on arterial oxygen saturation (SaO2), breathing patterns, electroencephalographic (EEG) sleep stage, and overnight change in FEV1 in 10 patients with stable asthma. After taking ketotifen, the patients slept longer and their sleep was less disturbed than after taking placebo, true sleep occupying 387 (SEM 8) minutes after ketotifen and 336 (19) minutes after placebo (p less than 0.02). On ketotifen nights the patients had less wakefulness and drowsiness (EEG sleep stages 0 and 1) and more non-rapid eye movement (non-REM) sleep than on placebo nights, but the duration of REM sleep was similar on the two occasions. Nocturnal changes in SaO2, the duration of irregular breathing, and overnight change in FEV1 were unaffected by ketotifen.

Adolescent↗
PubMed1983

Arterial oxygenation during sleep in patients with right-to-left cardiac or intrapulmonary shunts.

We have studied arterial oxygen saturation (SaO2), breathing patterns, and electroencephalographic (EEG) sleep stage during nocturnal sleep in six patients with right-to-left cardiac or intrapulmonary shunts and six patients with chronic bronchitis and emphysema, chosen because they were equally hypoxaemic when awake (SaO2 during wakefulness: bronchitis 74-90%, mean 83%; shunt 77-89%, mean 83%). The patients with bronchitis had far greater falls in SaO2 when asleep than those with shunts (maximum fall in SaO2 during sleep: bronchitis 14-47%, mean 29%; shunt 5-10%, mean 8%; p less than 0.01). Significant episodes of hypoxaemia (defined as SaO2 falls greater than 10%) occurred in all six bronchitic patients, from once to seven times per night, but in none of the patients with shunts (p less than 0.05). Twenty-four of the 27 episodes of hypoxaemia occurred in rapid-eye-movement (REM) sleep and 24 were associated with hypopnoea. The two groups of patients had similar EEG sleep patterns and the same amount of hypopnoea during sleep. Thus the level of arterial oxygenation when the patient is awake is not the sole determinant of the degree of nocturnal hypoxaemia; the pathological process is also important.

Adult↗
PubMed1983

Can right ventricular performance be assessed by equilibrium radionuclide ventriculography?

Although right ventricular function may be examined by following the passage (first pass) of a bolus of radionuclide through the right heart before it reaches the left heart, the counts detected with conventional gamma cameras in such a short time interval are low; moreover, repeated determinations would result in an unacceptable radiation burden to the patient. We have modified the gated equilibrium blood pool method to allow repeated assessment of the right ventricular ejection fraction (RVEF) and have compared the results with the first-pass method in 43 patients. Good agreement was obtained between the two methods (r = 0.91, p less than 0.001). The mean difference between the two methods was 0.04 with an intra-observer variation for the equilibrium studies of 0.03 and an inter-observer difference of 0.04. The mean difference in RVEF for seven patients studied on two separate occasions 30 minutes apart was only 0.02. In four patients the mean RVEF measured at rest was 0.44 +/- 0.05 (SEM) and after exercise it was 0.48 +/- 0.06. After infusion of isoprenaline at 1 microgram/min the mean rose to 0.64 +/- 0.04 (p less than 0.02) and after infusion of a new beta 1-sympathomimetic agent, prenalterol, at doses of 1 and 2 mg it was 0.56 +/- 0.02 (p less than 0.02) and 0.59 +/- 0.03 (p less than 0.01) respectively, where the significance levels are relative to the resting values. In nine patients with good ventricular function the vasodilator nifedipine caused right and left ventricular ejection fractions to increase by the same amount; while in six patients with severe impairment of left ventricular function due to ischaemic heart disease the RVEF increased from 0.58 +/- 0.03 to 0.73 +/- 0.03 (p less than 0.01) after 2 mg of prenalterol, but the left ventricular ejection fraction increased only from 0.22 +/- 0.04 to 0.26 +/- 0.04. We conclude that repeated estimation of right ventricular performance is possible by equilibrium radionuclide ventriculography.

Adrenergic beta-Agonists↗
PubMed1983

Assessment by radionuclide angiography of right and left ventricular function in chronic bronchitis and emphysema.

Non-invasive measurements of right and left ventricular ejection fraction (RVEF, LVEF) by multiple-gated equilibrium radionuclide ventriculography were performed in 18 control subjects, 16 patients with angina pectoris, and 45 patients with hypoxic chronic bronchitis and emphysema. The mean RVEF in the control subjects was 0.62 +/- 0.09 (SD), which was not significantly different from the mean RVEF in the patients with angina (0.60 +/- 0.09), but was significantly higher (p less than 0.01) than the mean value in patients with chronic bronchitis and emphysema (0.45 +/- 0.11). LVEF was not significantly different in the groups studied. There was a significant correlation between LVEF and RVEF only in patients with chronic bronchitis and emphysema (p less than 0.001). Those patients with chronic bronchitis and emphysema who had clinical evidence of cor pulmonale at the time of the study had significantly lower values of RVEF and LVEF (p less than 0.001) than patients with no previous cor pulmonale or those who had had cor pulmonale in the past. There was a significant correlation between RVEF and arterial oxygen (p less than 0.01) and carbon dioxide tensions (p less than 0.05). Reduced RVEF in patients with chronic bronchitis and emphysema may be an early indicator of the development of cor pulmonale and may be useful as a non-invasive method of assessing the effects of therapeutic interventions.

Adult↗
PubMed1983

Transient hypoxemia during sleep in chronic obstructive pulmonary disease is not a sleep apnea syndrome.

We measured ear oxygen saturation (SaO2), chest wall movement, and oronasal air flow, and took electroencephalographic tracings during nocturnal sleep in 20 healthy subjects and 20 similarly aged patients with chronic obstructive pulmonary disease (COPD), none of whom was obese. Thirteen of the patients with COPD were persistently hypoxemic and hypercapnic when awake ("blue and bloated", Type B); the remaining 7 maintained relatively normal arterial gas tensions when awake despite equally severe airways obstruction ("pink and puffing", Type A). Hypoxemic episodes (HE) (SaO2 falls of greater than 10%) occurred during sleep in all the blue bloaters but in only 3 of 7 pink puffers and 3 of 20 normal subjects. However, the maximal change in arterial oxygen tension (PaO2) (calculated from SaO2 values assuming normal pH) was similar in all 3 groups, averaging 24 mmHg. Furthermore, the cumulative duration of apnea and hypopnea was the same in each group. Only one patient COPD had more than 2 apneas per night, and obstructive apnea was seen only in the healthy subjects. Sleep apnea syndromes thus appear to be rare in nonobese patients with COPD. Of the 40 HE in patients with COPD, 29 occurred during periods of hypoventilation. In 10 blue bloaters whose arterial blood was sampled during sleep, the measured fall in PaO2 during the HE (mean, 11.2 mmHg) was greater than the rise in PaCO2 (mean, 4.2 mmHg). Although these changes in arterial gas tensions could be produced by an increase in ventilation-perfusion imbalance during the HE, it is suggested that unsteady-state gas exchange during transient hypoventilation could provide an alternative explanation.

Adult↗
PubMed1983

Long-term oxygen therapy--state of the art.

Long-term oxygen therapy prolongs life in adults with chronic hypoxia caused by chronic bronchitis and emphysema who have cor pulmonale, pulmonary hypertension, and secondary polycythemia ('blue bloaters'). Good results require oxygen therapy for more than 15 hours and preferably 20-24 hours per day. The oxygen concentrator, delivering 1 to 3 l/min of oxygen by nasal prongs, is probably the most cost-effective method of providing this therapy. Dangers of the therapy include fires and burning of patients who smoke, and this is a contraindication to treatment. Excessive CO2 retention during sleep should not result from controlled low-dose oxygen therapy unless the patient also has an obstructive sleep apnea syndrome. Oxygen therapy during sleep may prevent hypoxemic episodes in blue bloaters, and it may thus reverse their pulmonary hypertension, which probably potentiates the risk of right-heart failure and cor pulmonale.

Humans↗
PubMed1982

Irregular breathing and hypoxaemia during sleep in chronic stable asthma.

Breathing patterns, ear oxygen saturation (SaO2), and EEG sleep-stage throughout an undisturbed night's sleep were compared in ten adult stable asthmatics and ten age-matched healthy subjects. The two groups slept equally long (5.0-7.2, mean 6.2 h), but the asthmatics slept less well; they had more periods of wakefulness and drowsiness and irregular breathing than did the healthy subjects. They also had greater and more frequent falls in SaO2. Most hypoxaemic episodes occurred in the rapid-eye movement phase of sleep and were associated with hypopnoea or apnoea, but no patient had a classical sleep-apnoea syndrome. The severity of nocturnal hypoxaemia was related to the level of SaO2 when the subjects were awake, but did not correlate with the fall in forced expiratory volume recorded in eight out of ten asthmatics after sleep.

Adult↗
PubMed1982

Oxygen in the home.

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Home Care Services↗
PubMed1982

Preservation of the hypoxic drive to breathing in diabetic autonomic neuropathy.

1. Unexplained cardiorespiratory arrests have been reported in patients with diabetic autonomic neuropathy and these could be due to denervation of the carotid chemoreceptors. 2. We have studied the ventilatory response to transient hypoxia (Ve/Peto2) during exercise in 22 male diabetic patients, six with symptomatic and cardiovascular evidence to suggest diabetic autonomic neuropathy (DAN+) and 12 without these features (DAN-). 3. There was no difference in the ventilatory response to transient hypoxia between the different groups of diabetic patients (Ve/Peto2 in DAN+ patients = -0.9 +/- 0.2 litre min-1 kPa-1; Ve/Peto2 in DAN- patients = -1.2 +/- 0.6 litres min-1 kPa-1) even allowing for differences in the level of exercise achieved (CO2 production in DAN+ patients = 743 +/- 103 ml/min; CO2 production in DAN- patients = 800 +/- 144 ml/min). These results fell within our normal range for ventilatory response to transient hypoxia at this level of exercise. 4. The heart rate response to transient hypoxia varied within the groups but was significantly (P less than 0.05) less in the patients with established diabetic autonomic neuropathy. 5. We conclude that the peripheral chemoreceptors are intact in diabetic autonomic neuropathy and that other mechanisms must be implicated in the unexpected cardiorespiratory arrests seen in these patients.

Adult↗
PubMed1982

Night sleep of patients with chronic ventilatory failure and age matched controls: number and duration of the EEG episodes of intervening wakefulness and drowsiness.

Characteristics of the episodes of wakefulness and drowsiness (stage 0 + 1) intervening in a night of electrophysiologically monitored sleep were compared in a homogeneous group of 13 patients (mean age 57 years) with severe hypoxic chronic bronchitis and emphysema (blue and bloated variety) and 8 age matched control subjects. The total amounts of stage 0 + 1 accumulated over one night (preceded by one night of adaptation) were high in both groups (28% in the patients, 22% in the control subjects). A significant difference was found in the number of brief arousals (episodes of stage 0 + 1 lasting for less than 1 min), which averaged 10/h of sleep in the patients, and 6/h of sleep in the control subjects (p less than 0.05, two tailed). The numbers of longer episodes of stage 0 + 1 were not significantly different and varied independently from the numbers of brief arousals in the individuals. Only a small proportion (8 %) of brief arousals was linked to episodes of hypopnea or apnea in the bronchitic patients. Large numbers of brief arousals/h of non rapid eye movement sleep inthe bronchitic patients correlated significantly with small percentages of stage 3 + 4 sleep (p less than 0.05), and were associated with smell numbers of hypoxemic episodes occurring predominantly in rapid eye movement sleep. The findings indicate a more fractionated sleep in the patients with chronic hypoxic bronchitis, and suggest that the brief arousals represent a limiting factor rather than a result of the nocturnal hypoxemic episodes occurring in these patients.

Arousal↗