Changes in atrial natriuretic peptide concentrations during intravenous saline infusion in hypoxic cor pulmonale.

BACKGROUND: The pathogenesis of oedema in hypoxic cor pulmonale is poorly understood. One possibility is a failure of atrial natriuretic peptide release, leading to salt and water retention. This hypothesis was tested by observing the response to an intravenous saline challenge in patients with and without cor pulmonale. METHODS: Plasma atrial natriuretic peptide concentrations were measured before and for three hours after an intravenous saline load (0.1 ml 2.7% saline/kg/min for 60 minutes) in 20 patients with chronic obstructive airways disease. Ten patients with cor pulmonale, as judged clinically by the presence of peripheral oedema with a previously documented increase in the jugular venous pressure or pleural effusions during an acute exacerbation of airway obstruction (mean (SE) age 67 (3) years, FEV1 0.73 (0.08) 1, arterial oxygen tension (PaO2) 6.4 (0.4) kPa, and arterial carbon dioxide tension (PaCO2) 6.7 (0.3) kPa), were compared with 10 patients with hypoxic chronic obstructive airways disease who had never had oedema (mean age 63 (1) years, FEV1 1.07 (0.09) 1, PaO2 8.6 (0.4) kPa, and PaCO2 5.3 (0.2) kPa). All patients were studied fasting and after diuretics had been stopped for three days. No supplemental oxygen was given. RESULTS: The mean four hourly urine sodium excretion was less in the patients who had oedema (27 (4.6) mmol, 13% of the intravenous load) than in those without oedema (82 (15.5) mmol, 43% of the load). Initial mean plasma atrial natriuretic peptide values were significantly higher in the patients with cor pulmonale (19.1 (1.6) compared with 10.2 (0.7) pmol/l) and the mean peak rise in atrial natriuretic peptide after the intravenous saline load had been given was 13 (8.0) pmol/l in the patients with cor pulmonale and 5.5 (2.3) pmol/l in the controls. There were no significant differences in plasma and urinary osmolality, blood pressure, or creatinine clearance between the groups. CONCLUSION: Patients with chronic obstructive airways disease and cor pulmonale have an impaired ability to excrete a hypertonic intravenous saline load despite a normal physiological release of plasma atrial natriuretic peptide.     

Inhaled nitric oxide and arterial oxygen tension in patients with chronic obstructive pulmonary disease and severe pulmonary hypertension

BACKGROUND: Inhaled nitric oxide (NO) is a selective pulmonary vasodilator which can improve gas exchange in acute lung injury. However, it is uncertain that this effect on arterial oxygenation can be generalised to all lung diseases. METHODS: The effects of inhaled NO on gas exchange were studied in nine patients with chronic obstructive pulmonary disease (COPD), 11 patients with severe pulmonary hypertension, and 14 healthy volunteers. A randomized sequence of 40 ppm of NO or air was inhaled for 20 minutes through an orofacial mask. RESULTS: Inhaled NO reduced mean (SE) transcutaneous arterial oxygen tension (TcPO2) from 9.6 (0.3) to 8.9 (0.4) kPa in healthy volunteers and from 7.4 (0.6) to 7.0 (0.5) kPa in patients with COPD. There was no change in TcPO2 in patients with severe pulmonary hypertension. During inhalation of NO and air no change occurred in transcutaneous arterial carbon dioxide tension (TcPCO2), arterial oxygen saturation (SaO2) measured by pulse oximeter, or cardiac output determined by the transthoracic impedance method. CONCLUSIONS: Inhaled NO does not improve TcPO2 nor increase cardiac output in normal subjects and patients with COPD, suggesting that inhaled NO worsens gas exchange. This could represent inhaled NO overriding hypoxic pulmonary vasoconstriction in COPD. The finding that TcPO2 also fell when normal subjects inhaled NO suggests that a similar mechanism normally contributes to optimal gas exchange. Whilst inhaled NO can improve oxygenation, this effect should not be considered to be a general response but is dependent on the type of lung disease.


     

Oral almitrine in treatment of acute respiratory failure and cor pulmonale in patients with an exacerbation of chronic obstructive airways disease.

The effects of oral almitrine bismesylate, a respiratory stimulant that acts on peripheral arterial chemoreceptors, was studied in patients with chronic obstructive airways disease and hypoxaemic cor pulmonale. Twenty three patients admitted to hospital with an acute exacerbation of ventilatory failure were randomised to receive either almitrine 100 mg twice a day reducing to 50 mg twice a day over 48 hours or placebo in addition to conventional treatment. On admission the mean (SE) values for blood gas tensions were PaO2 4.8 (0.3) and PaCO2 7.7 (0.3) kPa in the 12 patients who received almitrine and PaO2 4.9 (0.1) and PaCO2 7.6 (0.3) kPa in the 11 who received placebo. After three hours of oxygen therapy at 1 1/min there was a similar rise in PaO2 in both groups, 6.4 (0.2) kPa in those receiving almitrine and 6.6 (0.4) kPa in those receiving placebo. After 24 hours of oxygen therapy values of PaO2 were again similar at 6.3 (0.8) kPa and 6.7 (2.2) kPa respectively. Arterial blood gas tensions improved during the study in those who survived but no significant differences were apparent between the two groups. There were six deaths, five in the almitrine group and one in the placebo group. There were no differences between the groups in respiratory rate, results of spirometry, oxygen requirement, or degree of dyspnoea (on visual analogue scale). The results did not show any benefit from oral almitrine in patients with acute respiratory failure secondary to chronic obstructive airways disease. Plasma almitrine concentrations, however, were often below the optimum therapeutic range, suggesting impaired drug absorption.     

The predictive value of transcutaneous oxygen tension measurement in diabetic lower extremity ulcers treated with hyperbaric oxygen therapy: a retrospective analysis of 1144 patients

The objective of this retrospective analysis was to determine the reliability of transcutaneous oxygen tension measurement (TcPO2) in predicting outcomes of diabetics who underwent hyperbaric oxygen therapy for lower extremity wounds. Six hyperbaric facilities provided TcPO2 data under several possible conditions: breathing air, breathing oxygen at sea level, and breathing oxygen in the chamber. Overall, 75.6% of the patients improved after hyperbaric oxygen therapy. Baseline sea-level air TcPO2 identified the degree of tissue hypoxia but had little statistical relationship with outcome prediction because some patients healed after hyperbaric oxygen therapy despite very low prehyperbaric TcPO2 values. Breathing oxygen at sea level was unreliable for predicting failure, but 68% reliable for predicting success after hyperbaric oxygen therapy. TcPO2 measured in chamber provides the best single discriminator between success and failure of hyperbaric oxygen therapy using a cutoff score of 200 mmHg. The reliability of in-chamber TcPO2 as an isolated measure was 74% with a positive predictive value of 58%. Better results can be obtained by combining information about sea-level air and in-chamber oxygen. A sea-level air TcPO2 < 15 mmHg combined with an in-chamber TcPO2 < 400 mmHg predicts failure of hyperbaric oxygen therapy with a reliability of 75.8% and a positive predictive value of 73.3%.     

Effect of L-arginine on renal blood flow in normal subjects and patients with hypoxic chronic obstructive pulmonary disease.

BACKGROUND: L-arginine is the precursor of endothelium derived nitric oxide (NO) and increasing the available substrate may increase the production of NO. This has been shown by local infusion in peripheral vascular beds but there are few studies of the effects during systemic infusion. Renal vasoconstriction is known to be important in the pathogenesis of cor pulmonale in patients with hypoxic chronic obstructive pulmonary disease (COPD). The effects of a systemic infusion of L-arginine on renal and aortic haemodynamics were therefore investigated in normal subjects and in patients with hypoxic COPD. METHODS: Ten normal volunteers were recruited from the research staff of King's College Hospital Six patients with COPD and hypoxia (arterial oxygen tension (PaO2) < 8.5 kPa) were recruited from the thoracic medicine outpatient clinic at King's College Hospital and five age and sex matched normal subjects were recruited from a group of normal subjects recruited from the database of the Department of Health Care for the Elderly as volunteers for medical research. There was no history of renal, cardiac, or hepatic disease. Baseline values of time averaged mean of the maximum instantaneous velocity (Tamx) and maximum velocity (Vmax) of blood flow in intrarenal arteries were obtained using colour flow Doppler ultrasound. Using the same technique, Vmax was obtained from the abdominal aorta just distal to the xiphisternum before and after infusion of L-arginine via a large peripheral vein (20 g in 100 ml sterile water over 30 minutes). RESULTS: In normal subjects L-arginine increased blood velocity in the intrarenal vessels from a mean of 0.22 m/s to 0.26 m/s, an increase of 19.8%. There was no effect on arterial blood pressure, heart rate, or aortic blood velocity. L-arginine had no effect on intrarenal or aortic blood velocity in patients with hypoxic COPD. In age matched controls L-arginine increased blood velocity in the intrarenal vessels from a mean of 0.20 m/s to 0.26 m/s, an increase of 36.8%. There was no effect on arterial blood pressure, heart rate, or aortic blood velocity. CONCLUSIONS: L-arginine, at the doses administered, increased renal blood flow, as assessed by renal arterial velocity. This effect was not seen in patients with hypoxic COPD but was present in age matched controls. This suggests that the abnormal renal vascular control seen in hypoxic patients with COPD may reflect a disturbance of the L-arginine/nitric oxide pathway.     

Twelve year clinical study of patients with hypoxic cor pulmonale given long term domiciliary oxygen therapy.

Patients presenting with chronic obstructive airways disease and hypoxic cor pulmonale were assessed during a period of clinical stability. Seventy two patients (53 male) with a mean age of 60 years were selected for long term oxygen therapy. Mean FEV1 was 0.78 l and forced vital capacity 1.9 l. The mean arterial oxygen tension (PaO2) was 6.1 kPa (46 mm Hg) and the mean arterial carbon dioxide tension (PCO2) 6.9 kPa (52 mm Hg). All patients had a PaO2 of less than 8.0 kPa (60 mm Hg) and 57 patients had a PCO2 of more than 6.0 kPa (45 mm Hg). Pulmonary haemodynamics were measured in 45 patients yielding the following mean values: pulmonary artery pressure 28.3 mm Hg; cardiac output 5.9 l min-1; total pulmonary vascular resistance 59.2 kPa l-1 S. Oxygen delivery systems, including 23 oxygen concentrators, were installed in the patients' homes. Flow rates were adjusted to raise PaO2 to more than 8.0 kPa (60 mm Hg) for at least 15 hours each day and close supervision was maintained. Overall five year survival was 62%, which is better than previously reported for this type of patient; but the 10 year survival was only 26% owing to an observed acceleration in death rate at about this time. Progressive disturbances of the pulmonary circulation were arrested. Mortality was associated with the severity of airflow obstruction, reflecting a continuing pathological process affecting the airways.     

Potassium studies in chronic obstructive airways disease.

Seventeen male patients with chronic obstructive airways disease in remission were separated into two groups according to arterial carbon dioxide tensions. Hypercapnia was associated significantly with hypoxia and increased red cell volume whereas normocapnia was not. Normocapnic patients were significantly lighter than those with hypercapnia. Total body potassium (TBK) measured by the whole body monitor was significantly low in two of the patients studied (P less than 0.005). The mean value for TBK for the normocapnic group as a whole was significantly low (P less than 0.005), but the mean value for the hypercapnic group was not. Serum potassium and erythrocyte potassium concentrations were normal even when TBK was low, and diuretics had no apparent influence on these potassium values. Of four patients (two in the series and two others) who had TBK measured after a recent episode of cor pulmonale, three had significantly low values. The only previous studies using a whole body monitor to measure TBK in chronic obstructive airways disease found no such low values, though other workers estimating exchangeable potassium by isotope dilution techniques had found evidence of gross potassium depletion. It is concluded that low TBK does indeed occur in patients with chronic obstructive airways disease and that gross depletion is more likely to follow an episode of cor pulmonale.     

Flap monitoring by transcutaneous PO2 and PCO2: importance of transcutaneous PCO2 in determining follow-up treatment for compromised free flaps

The authors conducted a two-part study to determine whether transcutaneous oxygen pressure (TcPO (2)) and transcutaneous carbon dioxide pressure (TcPCO (2)) can be used to monitor flap viability after transplantation. The first part was an animal study in which TcPO (2) and TcPCO (2) were measured in 10 epigastric island flaps subjected to arterial or venous ischemia. The second part was a clinical study in which both were measured in 27 free skin flaps. In the experimental study, TcPO (2) decreased to nearly 0 mmHg after 10 minutes of arterial and venous ischemia. TcPCO (2) increased to 100 mmHg after 60 minutes of either type of ischemia. In the clinical study, congestion was suspected in six flaps on the basis of clinical signs alone. Three congested flaps with TcPCO (2) more than 90 mmHg were selected for intervention. The remaining three congested flaps, with TcPCO (2) 80 mmHg or less, survived completely without further treatment. The TcPO (2) of all treated flaps and of the six flaps not requiring further treatment was 0 mmHg. Results of experimental study indicate that TcPO (2) is more sensitive than TcPCO (2) to flap ischemia. However, results of clinical study suggest that it is very hard to distinguish congested flaps from healthy flaps by TcPO (2) alone. The authors believe that a congested flap with a TcPCO (2) more than 90 mmHg requires further treatment.     

Assessment of oxygen supplementation during air travel.

BACKGROUND: The aim of this study was to simulate an in flight environment at sea level with a fractional inspired concentration of oxygen (FiO2) of 0.15 to determine how much supplemental oxygen was needed to restore a subject's oxygen saturation (SaO2) to 90% or to the level previously attained when breathing room air (FiO2 of 0.21). METHODS: Three groups were selected with normal, obstructive, and restrictive lung function. Using a sealed body plethysmograph an environment with an FiO2 of 0.15 was created and mass spectrometry was used to monitor the FiO2. Supplemental oxygen was administered to the patient by nasal cannulae. SaO2 was continuously monitored and recorded at an FiO2 of 0.21, 0.15, and 0.15 + supplemental oxygen. RESULTS: When given 2 l/m of supplemental oxygen all patients in the 15% environment returned to a similar SaO2 value as that obtained using the 21% oxygen environment. One patient with airways obstruction needed 3 l/m of supplemental oxygen to raise his SaO2 above 90%. CONCLUSIONS: This technique, which simulates an aircraft environment, enables an accurate assessment to be made of supplemental oxygen requirements.     

Hypoxaemia and release of endothelin-1.

BACKGROUND--Secretion of the vasoconstrictor peptide endothelin-1 from vascular endothelium is increased by various stimuli. Whether hypoxaemia affects plasma levels of endothelin-1 in humans is unknown, but this may be important in the haemodynamic response to hypoxaemia. The plasma endothelin-1 concentrations in hypoxaemic humans has therefore been measured. METHODS--Plasma levels of endothelin-1 were measured by specific radioimmunoassay in 10 control subjects at rest and following 30 minutes of acute hypoxaemia (SaO2 75-80%) induced by breathing a nitrogen/oxygen mixture, and in 10 patients with hypoxaemic cor pulmonale. RESULTS--The plasma endothelin-1 concentration in control subjects was increased from a mean (SE) of 0.90 (0.11) pmol/l at baseline to 2.34 (0.34) pmol/l during hypoxaemia. In patients with cor pulmonale the plasma endothelin-1 concentration was 2.96 (0.34) pmol/l, raised in comparison with control subjects at rest but similar to levels in controls during hypoxaemia. CONCLUSIONS--Plasma levels of endothelin-1 were increased by hypoxaemia in humans. The raised levels observed in patients with cor pulmonale may largely be attributable to the effects of hypoxaemia, although the pathophysiological significance of these observations remains to be established.     

Use of nitric oxide inhalation in chronic obstructive pulmonary disease

BACKGROUND: Inhalation of nitric oxide with oxygen could be a promising treatment in patients with chronic obstructive pulmonary disease (COPD) and pulmonary hypertension. However, the current methods of delivery of NO are cumbersome and unsuitable for long term use. The present study was undertaken to investigate the safety and efficacy of a mixture of nitric oxide (NO) and oxygen administered via a nasal cannula for 24 hours in patients with oxygen dependent COPD. METHODS: Twenty five parts per million (ppm) of NO was administered by inhalation combined with supplemental oxygen at a flow rate of 2 l/min via a nasal cannula for 24 hours to 11 ambulatory men with stable, oxygen dependent COPD. Room air with supplemental oxygen at 2 l/min was administered in an identical manner for another 24 hours as control therapy in a randomised, double blind, crossover fashion to all patients. Pulmonary function tests, exercise tolerance, dyspnoea grade, and lung volumes were measured at baseline, 24, and 48 hours. Pulmonary artery pressure (PAP), cardiac output (CO), pulmonary vascular resistance (PVR), arterial blood gas tensions, and minute ventilation were measured at baseline, after 30 minutes and 24 hours of breathing NO and oxygen. Venous admixture ratio (Qs/Qt) and dead space ratio (Vd/Vt) were also calculated. Concentrations of nitrogen dioxide (NO(2)) and NO in the inhaled and ambient air were monitored continuously. Differences in pulmonary function, arterial blood gas tensions, pulmonary haemodynamics, exercise tolerance, and dyspnoea between oxygen and NO breathing periods were analysed for significance using paired t tests. RESULTS: A significant (p<0.05) fall was observed in PVR (183.1 (116.05) and 137.2 (108.4) dynes.s.cm(-3) before and after breathing NO for 24 hours, respectively) with NO administration without significant changes in symptoms, pulmonary function, arterial oxygen tension, or exercise tolerance. CONCLUSIONS: NO at a concentration of 25 ppm blended with oxygen can be safely administered by nasal cannula for 24 hours without significant adverse effects and lowers PVR in stable patients with COPD receiving long term oxygen therapy.     

TcPO2 values in limb ischemia: effects of blood flow and arterial oxygen tension

Transcutaneous oxygen tension (TcPO2) is determined by blood flow and arterial oxygen tension (PaO2) and has been advocated as a measurement of tissue perfusion in peripheral vascular disease. The purpose of this study was to define the relationship between regional blood flow, PaO2, and TcPO2. TcPO2 sensors were placed on the skin of the anterior tibial regions of the hind limbs of 15 dogs. After occluding collateral blood flow, an external flow probe was placed around the femoral artery and an adjustable clamp was used to produce graded ischemia. Progressive reductions in blood flow were correlated with TcPO2 values at inspired oxygen concentrations (FiO2) of 0.21, 0.50, and 1.00. TcPO2 measured at room air decreased nonlinearly in relation to flow with a marked drop occurring below 20% of baseline flow. TcPO2 measured at increased FiO2 was dependent primarily on PaO2 at flow rates greater than 50% of baseline. With reduction in flow below 25% of baseline, TcPO2 was dependent solely on flow and was not augmented by increases in PaO2. The data suggest that TcPO2 can accurately reflect changes in blood flow to an extremity when flow is severely restricted.     

A review of microvascular measurements in wound healing

The microcirculatory evaluation in patients affected by arteriopathic or venous ulcers is usually carried out using laser Doppler flowmetry, transcutaneous oxygen (transcutaneous pressure of oxygen, TcPO(2)), and carbon dioxide (transcutaneous pressure of carbon dioxide, TcPCO(2)) measurements and capillaroscopy. These techniques provide significant pathophysiologic and prognostic information. TcPO(2) and TcPCO(2) diagnose and classify the extent of arterial disease in the leg ulcers caused by arterial disease; the prognostic value is recognized, though doubts about its prognostic potential exist in the case of leg ulcer. Laser Doppler flowmetry is able to identify the first functional impairment in the early stages of the arterial disease and in the complicated venous insufficiency. Capillaroscopy gives us morphological and quantitative parameters of the capillary bed that is damaged in arteriopathic and venous ulcers; nevertheless, it does not provide us with definite prognostic indexes. Combining the 3 methods may contribute to yield objective measures in the clinical management of lower extremity ulcers.     

Clinicopathological correlations in cor pulmonale.

BACKGROUND: The relation between pulmonary disease and physiological abnormality in patients with hypoxic cor pulmonale is controversial and the association between arterial hypoxaemia and right ventricular hypertrophy has been challenged. To address these problems matched patients treated with and without domiciliary oxygen were studied. METHODS: Necropsy data were obtained on 19 patients (14 male), 10 of whom had been treated with domiciliary oxygen. Pulmonary artery pressure and total pulmonary vascular resistance as well as blood gas tensions during the breathing of air and oxygen were available for the six months before death. Formalin fixed lung slices were assessed for panacinar and centriacinar emphysema. Right and left ventricular weights were measured and their ratio (LV&S/RV) was used as an index of right ventricular hypertrophy. Carotid body weights were available in 14 cases. RESULTS: Fourteen patients died of respiratory failure and antemortem thrombus was found in the pulmonary arteries of eight cases. Physiological measurements were unrelated to the degree of macroscopic emphysema, pulmonary hypertension, or daytime blood gas tensions. When allowance was made for the higher "ambient" arterial oxygen tension (PaO2) of those who had oxygen, PaO2 was correlated with LV&S/RV (r = 0.79), absolute right ventricular weight (r = -0.53), and carotid body weight (r = 0.68). CONCLUSIONS: These data show that in hypoxic cor pulmonale in vivo physiological disturbances are poor indicators of the underlying disease process. The relation of "ambient" PaO2 to right ventricular hypertrophy and carotid body weight suggests that domiciliary oxygen therapy might lead to regression of such established disease.     

Nocturnal hypoxaemia and quality of sleep in patients with chronic obstructive lung disease.

Fifty patients with chronic obstructive lung disease were questioned about their sleep quality and their responses were compared with those of 40 similarly aged patients without symptomatic lung disease. Patients with chronic obstructive lung disease reported more difficulty in getting to sleep and staying asleep and more daytime sleepiness than the control group. More than twice as many patients (28%) as controls (10%) reported regular use of hypnotics. In a subgroup of 16 patients with chronic obstructive lung disease (mean FEV1 0.88 (SD 0.44) sleep, breathing, and oxygenation were measured to examine the relationship between night time hypoxaemia and sleep quality. Sleep architecture was disturbed in most patients, arousals occurring from three to 46 times an hour (mean 15 (SD 14)/h). Arterial hypoxaemia during sleep was common and frequently severe. The mean (SD) arterial oxygen saturation (SaO2) at the onset of sleep was 91% (7%). Nine patients spent at least 40% of cumulative sleeping time at an SaO2 of less than 90% and six of these patients spent 90% of sleeping time below this level. Only four of 15 patients did not develop arterial desaturation during sleep. The mean minimum SaO2 during episodes of desaturation was less in rapid eye movement (REM) sleep (72% (17%)) than in non-REM sleep (78% (10%), p less than 0.05). The predominant breathing abnormality associated with desaturation was hypoventilation; only one patient had obstructive sleep apnoea. Arousals were related to oxygenation during sleep such that the poorer a patient's arterial oxygenation throughout the night the more disturbed his sleep (arousals/h v SaO2 at or below which 40% of the total sleep time was spent: r = 0.71, p less than 0.01). Hypoxaemia during sleep was related to waking values of SaO2 and PaCO2 but not to other daytime measures of lung function.     

Effect of simulated commercial flight on oxygenation in patients with interstitial lung disease and chronic obstructive pulmonary disease

BACKGROUND: Commercial aircraft cabins provide a hostile environment for patients with underlying respiratory disease. Although there are algorithms and guidelines for predicting in-flight hypoxaemia, these relate to chronic obstructive pulmonary disease (COPD) and data for interstitial lung disease (ILD) are lacking. The purpose of this study was to evaluate the effect of simulated cabin altitude on subjects with ILD at rest and during a limited walking task. METHODS: Fifteen subjects with ILD and 10 subjects with COPD were recruited. All subjects had resting arterial oxygen pressure (PaO2) of >9.3 kPa. Subjects breathed a hypoxic gas mixture containing 15% oxygen with balance nitrogen for 20 minutes at rest followed by a 50 metre walking task. Pulse oximetry (SpO2) was monitored continuously with testing terminated if levels fell below 80%. Arterial blood gas tensions were taken on room air at rest and after the resting and exercise phases of breathing the gas mixture. RESULTS: In both groups there was a statistically significant decrease in arterial oxygen saturation (SaO2) and PaO2 from room air to 15% oxygen at rest and from 15% oxygen at rest to the completion of the walking task. The ILD group differed significantly from the COPD group in resting 15% oxygen SaO2, PaO2, and room air pH. Means for both groups fell below recommended levels at both resting and when walking on 15% oxygen. CONCLUSION: Even in the presence of acceptable arterial blood gas tensions at sea level, subjects with both ILD and COPD fall below recommended levels of oxygenation when cabin altitude is simulated. This is exacerbated by minimal exercise. Resting sea level arterial blood gas tensions are similarly poor in both COPD and ILD for predicting the response to simulated cabin altitude.     

Hypoxaemia in chronic obstructive bronchitis.

Arterial blood gas tensions were studied for six years in 85 patients (59 men, 26 women, mean age 58.8 years) with hypoxaemia associated with chronic bronchitis. All patients who died had a precipitous fall of arterial oxygen tension (PaO2) breathing air. In patients dying within two years of the first appearance of ankle oedema the mean rate of fall of PaO2 was 0.11 kPa/month. Patients who survived two years appeared to deteriorate more slowly (0.017 kPa/month) until some months before death, when they too deteriorated rapidly. Hypoxaemic patients with obstructive airways disease suffer a terminal rapid decline in arterial oxygen tension, which probably indicates real pathological change in the lungs and has important implications for long-term domiciliary oxygen treatment.     

Prediction of oxygenation during sleep in patients with chronic obstructive lung disease.

The accuracy of a prediction equation for assessing the lowest arterial oxygen saturation (SaO2) during sleep was determined in 24 consecutive patients with chronic obstructive lung disease referred for assessment for home oxygen therapy. Subjects had a mean (SD) FEV1 of 0.81 (0.31) litre and an FEV1/FVC of 37% (12%). There was reasonable agreement between predicted and measured values (mean difference [predicted-measured] = -2.5%) but the prediction was not precise as the 95% confidence interval for the difference was +8% to -13%. The duration of arterial oxygen desaturation, defined as the percentage of total sleep time spent below a given SaO2, was not predicted accurately. It is concluded that nocturnal arterial oxygen desaturation in individual patients with chronic obstructive lung disease cannot be predicted from "awake" measurements with sufficient accuracy to be clinically useful.     

Evaluation of pulsed dose oxygen delivery during exercise in patients with severe chronic obstructive pulmonary disease

BACKGROUND: Oxygen conserving devices may lead to substantial increases in the duration of oxygen provided. A study was undertaken to compare the performance of a pulsed dose oxygen delivery (PDOD) system with continuous flow oxygen or air during a maximal walking test. METHODS: Fourteen patients with chronic obstructive pulmonary disease (COPD) and arterial oxygen desaturation on exercise (mean (SD) forced expiratory volume in one second (FEV1) 0.83 (0.28) 1, arterial oxygen pressure (PaO2) 8.38 (1.24) kPa, arterial carbon dioxide pressure (PaCO2) 5.95 (0.86) kPa) were randomised to perform a walking test using air administered via a cylinder or continuous flow oxygen at 2 l/min or by a PDOD system. RESULTS: There was no significant difference in the mean arterial oxygen saturation (SaO2) using the PDOD system or with continuous flow oxygen (p = 0.33). Patients showed greatest desaturation whilst walking with the air cylinder (SaO2 79.2 (8.59)%) which was significantly different from the desaturation with both continuous flow oxygen (87.6 (5.85)%, p = 0.001) and PDOD (85.6 (7.36)%, p = 0.004). There was no significant difference between the distance walked using oxygen delivered at 2 l/min by continuous flow or via the PDOD (p = 0.72; CI 0.34 to 1.08). The mean (SD) distance walked on continuous flow oxygen (203.6 (106.1) m) and PDOD (207.9 (109.8) m) was significantly greater than the distance walked with the air cylinder (188.6 (110.02) m); (1.12 fold increase in distance, CI 1.01 to 1.23, p = 0.02, and 1.14 fold increase in distance, CI 1.01 to 1.28, p = 0.03, respectively). CONCLUSIONS: These findings suggest that the pulsed dose oxygen conserving device was as effective as continuous flow oxygen in maintaining arterial oxygen saturation and that the use of this device was associated with similar improvements in exercise tolerance to patients taking continuous flow oxygen therapy.