Ventilation and gas exchange during sleep in patients with interstitial lung disease.

Ventilation and gas exchange during overnight sleep was studied in a group of seven patients with severe interstitial lung disease (mean vital capacity 50%, mean diffusing capacity 46% predicted), to see whether clinically significant oxygen desaturation occurred. Patients with a history of loud snoring or clinically significant airflow obstruction were excluded. Sleep was fragmented in these patients, but all achieved rapid eye movement (REM) sleep. All patients showed episodes of oxygen desaturation during sleep--mean (SEM) awake arterial oxygen saturation (SaO2) was 92.9% (0.3%) compared with a mean minimum SaO2 during sleep of 83.2% (2.1%) (p less than 0.01). These episodes were, however, transient, and mean SaO2 showed only a slight fall between wakefulness and sleep (non-REM 91.5%, REM 90.4%; NS). Furthermore, SaO2 during non-REM sleep correlated well (p less than 0.001) with SaO2 during wakefulness. Respiratory frequency showed a significant fall between wakefulness and sleep--21.1 (1.8) versus 17.3 (1.5) breaths per minute (p less than 0.02). Our data suggest that nocturnal oxygen treatment need not be considered in patients with interstitial lung disease unless the level of oxygenation while they are awake indicates the need for such treatment.     

Oxygen treatment of sleep hypoxaemia in Duchenne muscular dystrophy.

Patients with Duchenne muscular dystrophy develop progressive ventilatory muscle weakness and often die of respiratory complications. Recurrent, often profound, hypoxaemia has been shown in a previous study by this group to occur during rapid eye movement (REM) sleep in these patients before they develop sleep symptoms. In this study the efficacy and physiological effects of nocturnal oxygen in such patients have been assessed. Seven patients with Duchenne muscular dystrophy (age range 16-22 years; mean vital capacity 1.37 litres) with normal arterial blood gas tensions when awake were investigated by standard overnight polysomnography on an acclimatization night followed by two successive nights on which they received room air and nasal oxygen (2 litres/min) respectively in random order. Total sleep time, proportion of REM and non-REM sleep, and frequency and duration of arousals were similar on the two nights. When breathing air six of the seven subjects developed oxygen desaturation of more than 5% during REM sleep. With oxygen only one subject showed any oxygen desaturation exceeding 2.5%. Oxygen desaturation was associated with periods of hypopnoea or cessation of respiratory effort. The mean duration of episodes of hypopnoea and apnoea was prolonged during oxygen breathing by 19% and the mean duration of episodes during REM sleep by 33% (the proportion of REM sleep associated with hypopnoea and apnoea increased in all subjects). Heart rate in non-REM sleep fell by 9.3%; heart rate variation in REM and non-REM sleep was unchanged. These acute studies show that oxygen reduces the sleep hypoxaemia associated with respiratory muscle weakness; whether long term treatment will be possible or desirable is not clear as oxygen potentiates the underlying ventilatory disturbance.     

Patterns and predictors of sleep disordered breathing in primary myopathies

BACKGROUND: Sleep disordered breathing (SDB) is common in neuromuscular diseases but its relationship to respiratory function is poorly defined. A study was undertaken to identify distinct patterns of SDB, to clarify the relationships between SDB and lung and respiratory muscle function, and to identify daytime predictors for SDB at its onset, for SDB with continuous hypercapnic hypoventilation, and for diurnal respiratory failure. METHODS: Upright and supine inspiratory vital capacity (IVC, % predicted), maximal inspiratory muscle pressure (PImax), respiratory drive (P(0.1)), respiratory muscle effort (P(0.1)/PImax), and arterial blood gas tensions were prospectively compared with polysomnography and capnometry (PtcCO(2)) in 42 patients with primary myopathies. RESULTS: IVC correlated with respiratory muscle function and gas exchange by day and night. SDB evolved in three distinct patterns from REM hypopnoeas, to REM hypopnoeas with REM hypoventilation, to REM/non-REM (continuous) hypoventilation, and preceded diurnal respiratory failure. SDB correlated with IVC and PImax which yielded highly predictive thresholds for SDB onset (IVC <60%, PImax <4.5 kPa), SDB with continuous hypoventilation (IVC <40%, PImax <4.0 kPa), and SDB with diurnal respiratory failure (IVC <25%, PImax <3.5 kPa). CONCLUSION: Progressive ventilatory restriction in neuromuscular diseases correlates with respiratory muscle weakness and results in progressive SDB which, by pattern and severity, can be predicted from daytime lung and respiratory muscle function.     

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.     

Nocturnal saturation and respiratory muscle function in patients with chronic obstructive pulmonary disease.

BACKGROUND--Nocturnal desaturations, mainly caused by hypoventilation, occur frequently in patients with chronic obstructive pulmonary disease (COPD). Daytime arterial oxygen and carbon dioxide tensions (PaO2 and PaCO2) appear to predict which patients will desaturate at night. It is unknown if respiratory muscle strength, which may be decreased in these patients, plays an additional part. METHODS--Polysomnography, maximal respiratory pressures, lung function, and arterial blood gas tensions were measured in 34 patients with COPD (mean (SD) forced expiratory volume in one second (FEV1) 41.7 (19.9)% pred). RESULTS--Significant correlations were found between the mean nocturnal arterial oxygen saturation and maximal inspiratory mouth pressure (r = 0.65), maximal inspiratory transdiaphragmatic pressure (r = 0.53), FEV1 (r = 0.61), transfer coefficient (KCO) (r = 0.38), arterial oxygen saturation (SaO2) (r = 0.75), and PaCO2 (r = -0.44). Multiple regression analysis showed that 75% of the variance in nocturnal SaO2 (70%) and FEV1 (5%). CONCLUSION--Inspiratory muscle strength and nocturnal saturation data are correlated, but daytime SaO2 and FEV1 remain the most important predictors of nocturnal saturation.     

Prone position in mechanically ventilated patients with reduced intracranial compliance

BACKGROUND: Prone position has been used for several years to treat acute lung insufficiency, but in previous studies patients with unstable intracranial pressure (ICP) are mostly excluded. The aim of this study was to investigate if prone position is a safe and useful treatment in patients with reduced intracranial compliance. METHODS: A consecutive, prospective pilot study of 11 patients admitted to the neuro intensive care unit (NICU) due to traumatic brain injury or intracerebral haemorrhage. ICP, cerebral perfusion pressure (CPP), heart rate (HR), mean arterial blood pressure (MABP), arterial partial pressure of oxygen (PaO(2)), arterial partial pressure of carbon dioxide (PaCO(2)), arterial oxygen saturation (SaO(2)) and respiratory system compliance were measured before, three times during and two times after the patients were placed in the prone position. RESULTS: No significant changes were demonstrated in ICP, CPP or MABP. PaO(2) and SaO(2) were significantly increased in the prone position. HR was significantly increased in the prone position and after 10 min in the supine post-prone position and the respiratory system compliance was increased after 1 h in the supine post-prone position. CONCLUSION: Turning NICU patients from the supine to the prone position did not influence ICP, CPP or MABP, but significantly improved patient PaO(2), SaO(2) and respiratory system compliance.     

Comparison of almitrine bismesylate and medroxyprogesterone acetate on oxygenation during wakefulness and sleep in patients with chronic obstructive lung disease.

The effects of almitrine bismesylate and medroxyprogesterone acetate on oxygenation during wakefulness and sleep were compared in six patients with chronic obstructive lung disease and carbon dioxide retention. Patients received 1.5 mg/kg almitrine (a peripheral chemoreceptor stimulant), 100 mg of medroxyprogesterone (a central respiratory stimulant), or matched placebo daily for 15 days in random order in a crossover trial. When subjects were awake almitrine increased the ventilatory response to hypoxia and increased arterial oxygen tension (PaO2) to a greater extent than medroxyprogesterone, whereas medroxyprogesterone augmented the ventilatory response to hypercapnia and decreased arterial carbon dioxide tension (PaCO2) to a greater extent than almitrine. Neither drug influenced sleep architecture significantly, except that medroxyprogesterone increased the number of arousals. Almitrine had a more favourable effect than placebo on oxygenation as estimated from arterial oxygen saturation (SaO2) during the different stages of sleep, the number of episodes of hypoxaemia, and the amount of time that SaO2 was below 80%. The only change with medroxyprogesterone by comparison with placebo was a decrease in the number of hypoxaemic episodes. It is concluded that both active drugs improved blood gases during wakefulness, but that 1.5 mg/kg of almitrine is superior to 100 mg of medroxyprogesterone in improving SaO2 during sleep.     

Oxygen desaturation during sleep and exercise in patients with interstitial lung disease.

The relations between mean and maximum fall in arterial oxygen saturation (SaO2) during sleep, hypoxaemia during moderate and maximum exercise, and lung mechanics were studied in 16 patients with interstitial lung disease. Mean and minimum SaO2 during sleep were significantly related to each other and to daytime oxygenation but not to lung mechanics. Although the maximum fall in SaO2 during sleep was similar to the fall during maximum exercise (a level seldom achieved during normal daily activities), profound hypoxaemic episodes during sleep were rare and brief and therefore contributed little to the mean SaO2. The fall in mean SaO2 during sleep was not significant and was considerably less than during moderate exercise (average 0.5 v an estimated 4.5%, p less than 0.05). It is therefore concluded that in patients with interstitial lung disease oxygen desaturation during sleep is mild and less severe than hypoxaemia during exercise.     

Effects of acetazolamide in patients with the sleep apnoea syndrome.

There is as yet no convincing evidence that acetazolamide, a carbonic anhydrase inhibitor, is effective in obstructive sleep apnoea. A study was therefore designed to examine the effect of acetazolamide (250 mg/day) on sleep events and ventilatory control during wakefulness in nine patients with the sleep apnoea syndrome. In eight of the nine patients the apnoea index and the total duration of apnoea were reduced by acetazolamide, and the mean (SEM) apnoea index of all patients changed from 25.0 (6.7) to 18.1 (5.8) episodes an hour. Furthermore, the total time of arterial oxygen desaturation (SaO2)--more than 4% depression in SaO2 from the baseline sleeping level--divided by total sleep time was also significantly decreased and its mean (SEM) value improved from 24.1 (7.9) to 13.6 (4.8)% of total sleep time. Five of the seven patients with varying degrees of daytime hypersomnolence had their symptoms obviously improved. There was no patient whose predominant type of apnoea was converted from the obstructive to the central type, or vice versa. In the studies of wakefulness, metabolic acidosis, an increase of arterial oxygen tension (PaO2) and a decrease of arterial carbon dioxide tension (PaCO2) were observed. The slopes of the occlusion pressure response and the ventilatory response to carbon dioxide increased, and the carbon dioxide ventilatory response line shifted to the left. It is suggested that acetazolamide cannot remove apnoea completely but has a beneficial effect in mild cases of obstructive sleep apnoea through an augmentation of central (CO2, H+) drive and a stabilising effect on ventilatory control.     

Thoracoscopy: influence of the procedure on some respiratory and cardiac values

In eight patients with pleural effusion arterial oxygen and carbon dioxide tensions (PaO2 and PaCO2), pH, respiratory frequency, and cardiac rhythm and frequency were measured before, during, and after thoracoscopy. Four of the patients had a PaO2 below 70 mm Hg (9.3 kPa) before the procedure. During and after the procedure respiratory frequency increased and PaCO2 fell, indicating hyperventilation, while the other indices remained unchanged. It is concluded that respiration and the circulation readily adapt to the changes produced by the pneumothorax and the manipulation during thoracoscopy.     

Comparison of the transcutaneous oxygen and carbon dioxide tension in different electrode locations during general anaesthesia

BACKGROUND AND OBJECTIVE: The best place for the electrode of transcutaneous measurement of oxygen tension (tcPO2) and carbon dioxide tension (tcPCO2) during general anaesthesia was investigated in three different locations. METHODS: Fifteen patients for major abdominal surgery in the supine position were studied. The electrode of the TCM4 (Radiometer, Copenhagen, Denmark) was put on the chest, upper arm or forearm. TcPO2, tcPCO2, end-tidal carbon dioxide tension (etCO2), percutaneous oxygen saturation (SaO2), arterial oxygen tension (PaO2 ) and arterial carbon dioxide tension (PaCO2) were simultaneously measured at four different etCO2 concentrations and inhaled oxygen percentages and the location of the electrode was changed to other places to repeat the same measurement. In total, 12 measurements for each patient and 60 measurements for each place were performed. RESULTS: TcPO2 correlated better than SaO2 (R2 = 0.58) with PaO2 (R2 = 0.76), and tcPCO2 correlated well with PaCO2 (R2 = 0.76) and etCO2 (R2 = 0.74) when the electrode was put on the chest, while not on the upper arm or forearm (R2 < 0.5). However, limits of agreement were too big to use tcPO2 (bias, -67.9; limits of agreement, 16.5, -152.3) and tcPCO2 (bias, -0.47; limits of agreement, 8.7, -9.64) as surrogate measures of PaO2 and PaCO2, respectively even when the electrode was put on the chest. CONCLUSIONS: When the electrode was put on the chest, tcPO2 and tcPCO2 might be available as non-invasive monitors of oxygenation and CO2 status during general anaesthesia, while the absolute values were not interchangeable with PaO2 and PaCO2, respectively.     

A physiology simulator: validation of its respiratory components and its ability to predict the patient's response to changes in mechanical ventilation

We aimed to validate the mathematical validity and accuracy of the respiratory components of the Nottingham Physiology Simulator (NPS), a computer simulation of physiological models. Subsequently, we aimed to assess the accuracy of the NPS in predicting the effects of a change in mechanical ventilation on patient arterial blood-gas tensions. The NPS was supplied with the following measured or calculated values from patients receiving intensive therapy: pulmonary shunt and physiological deadspace fractions, oxygen consumption, respiratory quotient, cardiac output, inspired oxygen fraction, expired minute volume, haemoglobin concentration, temperature and arterial base excess. Values calculated by the NPS for arterial oxygen tension and saturation (PaO2 and SaO2), mixed venous oxygen tension and saturation (PvO2 and SvO2), arterial and mixed venous carbon dioxide tension (PaCO2 and PvCO2) and arterial pH were accurate compared with measured values. Subsequently, arterial gas responses to changes in minute volume of FiO2 were measured in 31 patients and were compared with the NPS prediction for each response. The 95% limits of agreement in predicting the magnitude of change were: arterial oxygen tension -2.07 to 2.47 kPa; PaCO2 -0.33 to 0.67 kPa; and pH -0.023 to 0.033. This investigation has validated respiratory components of the NPS. We recommend the NPS as a clinical tool for predicting the effects of alterations in mechanical ventilation in stable patients in the intensive care unit.      

Arterial blood gas analysis or oxygen saturation in the assessment of acute asthma?

BACKGROUND--A study was undertaken to determine if arterial blood gas estimation is always necessary in the assessment of patients presenting to hospital with acute severe asthma, or whether oxygen saturation as measured by pulse oximetry is a reliable screening test for predicting those in respiratory failure. METHODS--A prospective study was conducted in a specialist respiratory medical unit. Arterial blood gas tensions and pulse oximetry were measured in 89 consecutive patients admitted with acute severe asthma. Respiratory failure was defined as PaO2 < 8.0 kPa or PaCO2 > 6 kPa. RESULTS--When oxygen saturation was 92% or higher (72 patients) respiratory failure was found in three (4.2%) cases. In the 82 patients with a saturation of 90% or higher six patients (7.3%) had respiratory failure. CONCLUSIONS--In the initial assessment of acute severe asthma an oxygen saturation of > 92% suggests that respiratory failure is unlikely and therefore arterial blood gas measurement is unnecessary. This study is only relevant to the assessment of asthmatic patients at presentation. Other parameters of severity must be continually assessed in all asthmatic patients admitted to hospital irrespective of the initial SaO2, and blood gases measured when clinically indicated.     

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.     

Pulmonary arterial hypertension in patients with sleep apnoea syndrome

BACKGROUND: Pulmonary arterial hypertension (PAH) in patients with sleep apnoea syndrome (SAS) is classically ascribed to associated chronic obstructive pulmonary disease (COPD). The aim of this retrospective study was to evaluate the possible occurrence of PAH as a complication of SAS in patients without COPD. METHODS: Right heart catheterisation was performed in 44 patients with SAS and without COPD confirmed by polysomnography (apnoea index >5/h) admitted for the administration of nasal continuous positive airway pressure (CPAP). RESULTS: Precapillary PAH, defined as mean pulmonary arterial pressure of >20 mm Hg with pulmonary capillary wedge pressure <15 mm Hg, was observed in 12/44 (27%) patients with SAS. There were no significant differences in apnoea index between patients with (PAH+) and those without PAH (PAH-) (42.6 (26.3) versus 35.8 (21.7) apnoeas/h). The PAH+ group differed significantly from the PAH- group in the following respects: lower daytime arterial oxygen tension (PaO(2)) (9.6 (1.1) versus 11.3 (1.5) kPa, p=0.0006); higher daytime arterial carbon dioxide tension (PaCO(2)) (5.8 (0.5) versus 5.3 (0.5) kPa, p=0.002); more severe nocturnal hypoxaemia with a higher percentage of total sleep time spent at SaO(2) <80% (32.2 (28.5)% versus 10.7 (18.8)%, p=0.005); and higher body mass index (BMI) (37.4 (6) versus 30.3 (6.7) kg/m(2), p=0.002). The PAH+ patients had significantly lower values of vital capacity (VC) (87 (14)% predicted versus 105 (20)% predicted, p=0.005), forced expiratory volume in one second (FEV(1)) (82 (14)% predicted versus 101 (17)% predicted, p=0.001), expiratory reserve volume (40 (16)% predicted versus 77 (41)% predicted, p=0.003), and total lung capacity (87 (13)% predicted versus 98 (18)% predicted, p=0.04). Stepwise multiple regression analysis showed that mean pulmonary artery pressure (PAPm) was positively correlated with BMI and negatively with PaO(2). CONCLUSION: Pulmonary arterial hypertension is frequently observed in patients with SAS, even when COPD is absent, and appears to be related to the severity of obesity and its respiratory mechanical consequences.     

Sleep hypoxia in myotonic dystrophy and its correlation with awake respiratory function.

BACKGROUND--Tiredness and daytime respiratory failure occur frequently in myotonic dystrophy. Sleep hypoxaemia was studied in 12 patients with myotonic dystrophy and correlations were sought with their daytime lung and respiratory muscle function. METHODS--All patients underwent overnight sleep studies, clinical assessment, measurement of flow-volume loops and carbon monoxide transfer factor, arterial blood gas analysis, and physiological assessment of both thoracic muscle function and upper airways obstruction. RESULTS--The mean nadir of oxygen saturation during sleep was 75% (95% confidence interval 69% to 81%). A mean of 3.4% of total sleep duration was spent at an oxygen saturation level below 85%. Five of the 12 patients had an apnoea index of > 5, the group mean apnoea/hypopnoea index being 15.8 events/sleep hour. The mean awake arterial oxygen tension (PaO2) was 10.7 kPa. There was a trend to hypercapnoea with a mean awake arterial carbon dioxide tension of 6.1 kPa; carbon dioxide retention worsened during sleep. Respiratory muscle dysfunction was mainly evident as a low maximum expiratory mouth pressure. Upper airway obstruction assessed by physiological criteria was found in four of the 12 patients. The proportion of total sleep duration with oxygen saturation levels below 85% was directly related to body mass index (weight/height2) and inversely related to the awake PaO2. Body mass index was inversely related to the overnight nadir of oxygen saturation. CONCLUSIONS--Patients with myotonic dystrophy are often hypoxic during sleep and the subgroup that are obese, or have symptoms of sleep apnoea, or both, are particularly at risk. Sleep studies should be considered in this subgroup of patients with myotonic dystrophy.     

Changes in day and night time oxygenation with protriptyline in patients with chronic obstructive lung disease.

The effect of protriptyline, a tricyclic antidepressant, on sleep architecture, nocturnal arterial oxygen desaturation, pulmonary function, and diurnal arterial blood gases was investigated in an open study of 14 patients with stable chronic obstructive lung disease. Daytime and overnight measurements were made before and 2 and 10 weeks after they started protriptyline (20 mg daily at bedtime). Two patients had to be excluded before the second visit and one before the third visit because of changes in treatment for their chest disease. Protriptyline caused mouth dryness in all patients and dysuria in six men. With protriptyline there were no significant changes in total sleep time, sleep period time, or the percentages of total sleep time occupied by stage I-II and stage III-IV sleep. The mean (SEM) percentage of total sleep time spent in rapid eye movement (REM) sleep decreased from 11.1 (1.7) to 4.6 (0.7) at two weeks and to 4.2 (1.0) at 10 weeks. After protriptyline the time spent during sleep with an arterial oxygen saturation (SaO2) below each 5% increment above 65% was less than the baseline time; the lowest SaO2 (%) reached during sleep increased from 64.5 (1.7) to 72.7 (2.1) at 2 weeks and to 77.4 (2.1) at 10 weeks. Lung volumes and expiratory flows were unchanged during the study. Daytime arterial oxygen tension (PaO2) increased from 57 (1.4) mm Hg before treatment to 62 (1.9) mm Hg at 2 weeks and to 66 (1.9) mm Hg at 10 weeks (7.6 (0.2), 8.3 (0.3), 8.8 (0.3) kPa). Carbon dioxide tension fell from 52 (2.3) mm Hg to 49 (1.4) mm Hg at 2 weeks and to 48 (2.0) mm Hg at 10 weeks (6.9 (0.3), 6.5 (0.2), 6.4 (0.3) kPa), but these changes were not significant. These results suggest that protriptyline may benefit patients with chronic obstructive lung disease by reducing the sleep induced falls in SaO2 and improving diurnal PaO2; a controlled trial is now required.     

High-frequency percussive ventilation as a salvage modality in adult respiratory distress syndrome: a preliminary study

Despite multiple advances in critical care patients with severe adult respiratory distress syndrome (ARDS) can exhaust the capability of conventional ventilation; this results in respiratory failure and death. High-frequency percussive ventilation (HFPV), which was initially utilized for salvage of burn patients with smoke inhalation injury refractory to conventional ventilation, has evolved as a standard of burn care. Based on our experience with HFPV in burn patients the burn team was consulted to provide salvage ventilation for non-burn surgical intensive care unit patients with refractory respiratory failure. Over a 14-month period ten patients with refractory ARDS from multiple causes were treated. Retrospective chart review was performed. Respiratory parameters were assessed before and 24 hours after initiation of HFPV. Mean values of fraction of inspired oxygen (FiO2), pH, partial pressure of O2 in arterial blood (PaO2), partial pressure of CO2 in arterial blood (PaCO2), HCO3, oxygen saturation in arterial blood (SaO2), PaO2/FiO2, and peak inspiratory pressure were compared. Significant improvement in oxygenation was reflected by increases in SaO2, PaO2, and the PaO2/FiO2 ratio in the first 24 hours of HFPV. No significant increase in peak inspiratory pressure was documented by conversion from conventional ventilation to HFPV. No hemodynamic changes directly associated with HFPV were noted. Seven of ten patients failing conventional ventilation survived to hospital discharge after salvage therapy with HFPV. We advocate further studies of HFPV in non-burn patients with ARDS both as salvage therapy and as replacement for conventional ventilation for the initial treatment for ARDS.     

Role of hypoxia on increased blood pressure in patients with obstructive sleep apnoea.

BACKGROUND--Cyclical changes in systemic blood pressure occur during apnoeic episodes in patients with obstructive sleep apnoea (OSA). Although several factors including arterial hypoxaemia, intrathoracic pressure changes, and disruption of sleep architecture have been reported to be responsible for these changes in blood pressure, the relative importance of each factor remains unclear. This study assessed the role of hypoxaemia on the increase in blood pressure during apnoeic episodes. METHODS--The blood pressure in apnoeic episodes during sleep and the blood pressure response to isocapnic intermittent hypoxia whilst awake were measured in 10 men with OSA. While asleep the blood pressure was measured non-invasively using a Finapres blood pressure monitor with polysomnography. The response of the blood pressure to hypoxia whilst awake was also measured while the subjects intermittently breathed a hypoxic (5% or 7% oxygen) gas mixture. Each hypoxic gas exposure was continued until a nadir arterial oxygen saturation (nSaO2) of less than 75% was reached, or for a period of 100 seconds. The exposure was repeated five times in succession with five interposed breaths of room air in each run. RESULTS--The mean (SD) increase in blood pressure (delta MBP) during apnoeic episodes was 42.1 (17.3) mm Hg during rapid eye movement (REM) sleep and 31.9 (12.5) mm Hg during non-REM sleep. The delta MBP during apnoeic episodes showed a correlation with the decrease of nSaO2 (delta SaO2) (r2 = 0.30). The change in blood pressure in response to intermittent hypoxia whilst awake was cyclical and qualitatively similar to that during apnoeic episodes. Averaged delta MBP at an SaO2 of 7% and 5% oxygen was 12.6 (5.7) and 13.4 (3.6) mm Hg, respectively, whereas the averaged delta MBP at the same delta SaO2 during apnoeic episodes was 38.4 (15.5) and 45.2 (20.5) mm Hg, respectively. CONCLUSIONS--The blood pressure response to desaturation whilst awake was about one third of that during apnoeic episodes. These results suggest that factors other than hypoxia may play an important part in raising the blood pressure during obstructive sleep apnoea.     

Arterial oxygenation changes in valvular heart disease patients with cardiomegaly in different recumbent positions

BACKGROUND AND OBJECTIVE: We studied the effect of different recumbent positions (supine, left and right lateral decubitus), on arterial oxygenation in 42 valvular heart disease patients planned for cardiac surgery. All patients had cardiomegaly (cardiothoracic ratio > or = 0.5) in their chest X-rays. Their left ventricular end-diastolic diameter was also noted from the preoperative echocardiogram. METHODS: Arterial blood gas analysis was performed in supine, left and right lateral positions after keeping the patient in a given position for 15 min. During this period all patients received 35% oxygen supplementation. RESULTS: Arterial oxygen tension and haemoglobin saturation were significantly higher in the right lateral position (PaO2 = 120.6 +/- 29.5 mmHg, SaO2 = 98.1 +/- 1.4%) than in supine (PaO2 = 111.0 +/- 30.6 mmHg, SaO2 = 97.6 +/- 2.2%) and left lateral positions (PaO2 = 109.7 +/- 32.0 mmHg, SaO2 = 97.6 +/- 1.7%; mean +/- SD; P 0.05). The change in PaO2 and SaO2 with change of posture from left to right was significantly related to left ventricular end-diastolic diameter (r = 0.50 and r = 0.63, respectively; Pearson correlation). Repeated measures of analysis of variance with left ventricular end-diastolic diameter as a covariate showed a significant change in arterial PaO2 with posture (P = 0.011). CONCLUSION: Right lateral posture improves arterial oxygenation in the valvular heart disease patient with an enlarged left ventricle. In the preoperative period, these patients may benefit from a right lateral posture when lying in bed.