Hypercapnic Patients Research Articles

Remifentanil Improves Breathing Pattern and Reduces Inspiratory Workload in Tachypneic Patients

Properly titrated opiates decrease respiratory rate but do not affect tidal volume or induce respiratory acidosis. To determine whether remifentanil improves breathing pattern or reduces inspiratory effort in patients with acute respiratory failure and tachypnea or rapid shallow breathing. We studied 14 patients who developed tachypnea and/or rapid shallow breathing if the pressure support level was reduced. During pressure support ventilation, each patient received 30-min infusions, separated by 30 min, of remifentanil and placebo. Measurements were obtained before commencing and before stopping each infusion, and after 3 min of unassisted breathing. The main outcomes were rapid shallow breathing index and change in pressure-time product. Remifentanil did not significantly affect tidal volume. During pressure support ventilation, remifentanil infusion reduced respiratory rate, pressure-time product, and cardiovascular double product (heart rate × systolic arterial pressure) without modifying the sedation score. Mean P(aCO(2)) showed a small and clinically negligible increase during remifentanil, but P(aCO(2)) increased more in the hypercapnic patients than in the normocapnic patients. Remifentanil reduced the rapid shallow breathing index after 3 min of unassisted breathing. Remifentanil improved respiratory pattern and decreased inspiratory muscles effort in patients with tachypnea or rapid shallow breathing, but did not affect oxygenation or sedation. Though the acid-base balance did not show clinically relevant changes on average, we cannot exclude the possibility that remifentanil might prolong weaning in hypercapnic patients. (Clinical-Trials.gov registration NCT00665119.)

Investigation of pulmonary hemodynamics and chest X-ray findings in hypercapnic patients with pulmonary tuberculosis sequelae

We investigated pulmonary hemodynamics and chest X-ray findings to explore pathophysiological significance of chronic hypercapnia in patients with pulmonary tuberculosis sequelae. One hundred and seven patients underwent examinations of blood gases and right cardiac catheterization. The patients were divided into two groups, according to arterial carbon dioxide tension under room air breathing (PaCO2). Group I (n = 35) was defined as 45 Torr or lower of PaCO2, and Group II (n = 72) was the hypercapnic group whose PaCO2 was over 45 Torr. In addition, spirometry was done in 34 patients of Group I and 68 of Group II. First, the values of blood gases, spirometry and pulmonary hemodynamics were compared between the two groups. Secondly, between 22 of Group I and 50 of Group II, the values of pulmonary arteriolar resistance (PAR) before and after 100% oxygen breathing for 10 minutes were compared. These comparisons were made by exploratory data analysis. Lastly, we described in all cases with five items of chest X-ray findings and the extent of each finding we had defined. The items were emphysematous change; fibrosis, bronchiectasis, and/or cavity (hereafter abbreviated as "fibrosis"); lung resection and/or atelectasis; pleural thickening; and thoracoplasty. We explored the items of X-ray findings which may relate to hypercapnia by ridit (abbreviation for "relative to an identified distribution") analysis. The results were as follows. (1) Hypercapnic patients tended to have severer restrictive ventilatory impairment and hypoxemia. Under an even level of arterial oxygen tension (PaO2), tissue oxygenation was not poorer in Group II than in Group I. (2) Hypercapnic patients tended to have more unfavorable pulmonary hemodynamics. More than half of them had pulmonary hypertension defined as 20 mmHg or higher of pulmonary artery mean pressure (PAm). Under an even level of PaO2, PAm was higher in Group II. Although 34 patients of Group II showed PaO2 over 60 Torr, 23 of them had pulmonary hypertension. (3) PAR after oxygen breathing was more likely to decrease in Group II than in Group I. (4) As any mean ridit was standardized and adjusted to 0.5 in Group I, the maximum was the mean ridit of "pleural thickening" (= 0.67), next "fibrosis" (= 0.65) in Group II. The above two items of X-ray findings, in which each mean ridit was higher than in any other item, were more influential on hypercapnia. We conclude as follows. (1) Pulmonary hypertension is severer in hypercapnic patients with pulmonary tuberculosis sequelae; it may be mainly attributable to hypoxic pulmonary vasoconstriction. (2) An important cause of chronic hypercapnia may be pathological changes such as "pleural thickening" and "fibrosis" seen on the radiogram.

The Effect of Supplemental Oxygen on Hypercapnia in Subjects With Obesity-Associated Hypoventilation: A Randomized, Crossover, Clinical Study

It is unknown whether oxygen therapy causes worsening hypercapnia in patients with obesity-associated hypoventilation (OAH), similar to the response observed in COPD. The objectives of this study were to investigate whether breathing 100% oxygen results in an increase in hypercapnia in patients with OAH and the mechanisms of any effect.In this double-blind, randomized, controlled, crossover trial, 24 outpatients with newly diagnosed OAH inhaled 100% oxygen or room air for 20 min on 2 separate days. Transcutaneous CO(2) tension (Ptco(2)), minute ventilation, and volume of dead space to tidal volume ratio were measured at baseline and at 20 min. A mixed linear model was used to determine differences between the two treatments.The study was terminated in three subjects breathing 100% oxygen due to a Ptco(2) increase ≥ 10 mm Hg, which occurred after 10:35, 13:20, and 15:51 min. Ptco(2) increased by 5.0 mm Hg (95% CI, 3.1-6.8; P < .001) with oxygen compared with room air. Minute ventilation decreased by 1.4 L/min (95% CI, 0.11-2.6 L/min; P = .03), and volume of dead space to tidal volume ratio increased by 0.067 (95% CI, 0.035-0.10; P < .001) with oxygen compared with room air.Breathing 100% oxygen causes worsening hypercapnia in stable patients with OAH.Australia New Zealand Clinical Trials Registry; No.: ACTRN 12608000592347; URL: www.anzctr.org.au.

Year in review 2010: Interstitial lung diseases, acute lung injury, sleep, physiology, imaging, bronchoscopic intervention and lung cancer

Year in review 2010: Interstitial lung diseases, acute lung injury, sleep, physiology, imaging, bronchoscopic intervention and lung cancer

Slow wave sleep in patients with respiratory failure

Background Slow wave sleep (SWS) has been theorized as reflecting a homeostatic sleep process and is considered a state of recuperation. SWS is reduced in obstructive sleep apnea (OSA) patients, but SWS has not been specifically studied in respiratory failure patients. The aim of this study is to investigate SWS in predominantly hypercapnic respiratory failure patients. Methods We analyzed sleep and arterial blood gas records of all 97 respiratory failure patients who underwent polysomnography and bilevel non-invasive ventilation (NIV) treatment in our laboratory from 2008 to July 2009. We also analyzed 32 initial diagnostic study data from these 97 patients. Results The 97 patients had an average age of 58 ± 15 (SD) years. Total sleep time was 320.3 ± 82.8 (SD) min of which 32.9% ± 15.4 (%) was spent in SWS. This high percentage SWS correlated positively with awake arterial CO 2 pressure (PCO 2) in both the 97 treatment studies ( r = 0.35, p = 0.001) and the 32 initial diagnostic studies ( r = 0.40, p = 0.025). The relationship was particularly apparent in patients with obesity hypoventilation syndrome or overlap syndrome. Statistical modelling identified three significant predictor variables for SWS across both diagnostic and NIV nights: PCO 2, arousal index and female gender. Conclusions Patients with respiratory failure have a high percentage of EEG assessed SWS which is in part determined by disease specific variables such as hypercapnia as well as by traditional SWS determinants such as sleep fragmentation and gender.

Sleeping on a Royal Flush

Sleeping on a Royal Flush

Influence of Diaphragmatic Mobility on Hypercapnia in Patients with Chronic Obstructive Pulmonary Disease

A reduction in diaphragm mobility has been identified in patients with chronic obstructive pulmonary disease (COPD) and has been associated with a decline in pulmonary function parameters. However, little information exists regarding the potential role of diaphragm mobility on hypercapnia in COPD. A new method of assessing the mobility of the diaphragm, using ultrasound, has recently been validated. The purpose of the present study was to investigate the relationship between diaphragm mobility and pulmonary function parameters, as well as that between arterial blood gas values and diaphragm mobility, in COPD patients. Thirty seven COPD patients were recruited for pulmonary function test, arterial blood gas analysis and diaphragm mobility using ultrasound to measure the craniocaudal displacement of the left branch of the portal vein. There were significant negative correlations between diaphragmatic mobility and PaCO2 (r = -0.373, P = 0.030). Diaphragmatic mobility correlated with airway obstruction (FEV1, r = 0.415, P = 0.011) and with ventilatory capacity (FVC, r = 0.302, P = 0.029; MVV, r = 0.481, P = 0.003). Diaphragmatic mobility also correlated significantly with pulmonary hyperinflation. No relationship was observed between diaphragm mobility and PaO2 (r = -0.028, P = 0.873). These findings support a possibility that the reduction in diaphragm mobility relates to hypercapnia in COPD patients.

The effects of long-term noninvasive ventilation in hypercapnic COPD patients: a randomized controlled pilot study

IntroductionNoninvasive ventilation (NIV) is a well-established treatment for acute-on- chronic respiratory failure in hypercapnic COPD patients. Less is known about the effects of a long-term treatment with NIV in hypercapnic COPD patients and about the factors that may predict response in terms of improved oxygenation and lowered CO2 retention.MethodsIn this study, we randomized 15 patients to a routine pharmacological treatment (n = 5, age 66 [standard deviation ± 6] years, FEV1 30.5 [±5.1] %pred, PaO2 65 [±6] mmHg, PaCO2 52.4 [±6.0] mmHg) or to a routine treatment and NIV (using the Synchrony BiPAP device [Respironics, Inc, Murrsville, PA]) (n = 10, age 65 [±7] years, FEV1 29.5 [±9.0] %pred, PaO2 59 [±13] mmHg, PaCO2 55.4 [±7.7] mmHg) for 6 months. We looked at arterial blood gasses, lung function parameters and performed a low-dose computed tomography of the thorax, which was later used for segmentation (providing lobe and airway volumes, iVlobe and iVaw) and post-processing with computer methods (providing airway resistance, iRaw) giving overall a functional image of the separate airways and lobes.ResultsIn both groups there was a nonsignificant change in FEV1 (NIV group 29.5 [9.0] to 38.5 [14.6] %pred, control group 30.5 [5.1] to 36.8 [8.7] mmHg). PaCO2 dropped significantly only in the NIV group (NIV: 55.4 [7.7] → 44.5 [4.70], P = 0.0076; control: 52.4 [6.0] → 47.6 [8.2], NS). Patients actively treated with NIV developed a more inhomogeneous redistribution of mass flow than control patients. Subsequent analysis indicated that in NIV-treated patients that improve their blood gases, mass flow was also redistributed towards areas with higher vessel density and less emphysema, indicating that flow was redistributed towards areas with better perfusion. There was a highly significant correlation between the % increase in mass flow towards lobes with a blood vessel density of >9% and the increase in PaO2. Improved ventilation–perfusion match and recruitment of previously occluded small airways can explain the improvement in blood gases.ConclusionWe can conclude that in hypercapnic COPD patients treated with long-term NIV over 6 months, a mass flow redistribution occurs, providing a better ventilation–perfusion match and hence better blood gases and lung function. Control patients improve homogeneously in iVaw and iRaw, without improvement in gas exchange since there is no improved ventilation/perfusion ratio or increased alveolar ventilation. These differences in response can be detected through functional imaging, which gives a more detailed report on regional lung volumes and resistances than classical lung function tests do. Possibly only patients with localized small airway disease are good candidates for long-term NIV treatment. To confirm this and to see if better arterial blood gases also lead to better health related quality of life and longer survival, we have to study a larger population.

Non-invasive pressure support ventilation and CPAP in cardiogenic pulmonary edema: a multicenter randomized study in the emergency department

Noninvasive pressure support ventilation (NIPSV) and continuous positive airway pressure (CPAP) are both advocated in the treatment of cardiogenic pulmonary edema (CPE); however, the superiority of one technique over the other has not been clearly demonstrated. With regard to its physiological effects, we hypothesized that NIPSV would be better than CPAP in terms of clinical benefit. In a prospective, randomized, controlled study performed in four emergency departments, 200 patients were assigned to CPAP (n = 101) or NIPSV (n = 99). Primary outcome was combined events of hospital death and tracheal intubation. Secondary outcomes included resolution time, myocardial infarction rate, and length of hospital stay. Separate analysis was performed in patients with hypercapnia and those with high B-type natriuretic peptide (>500 pg/ml). Hospital death occurred in 5 (5.0%) patients receiving NIPSV and 3 (2.9%) patients receiving CPAP (p = 0.56). The need for intubation was observed in 6 (6%) patients in the NIPSV group and 4 (3.9%) patients in the CPAP group (p = 0.46). Combined events were similar in both groups. NIPSV was associated to a shorter resolution time compared to CPAP (159 ± 54 vs. 210 ± 73 min; p < 0.01), whereas the incidence of new myocardial infarction was not different between both groups. Similar results were found in hypercapnic patients and those with high B-type natriuretic peptide. During CPE, NIPSV accelerates the improvement of respiratory failure compared to CPAP but does not affect primary clinical outcome either in overall population or in subgroups of patients with hypercapnia or those with high B-type natriuretic peptide.

Noninvasive Ventilation for COPD: Volume Assurance not very Reassuring

Noninvasive ventilation (NIV) to treat severe COPD was first proposed over 50 years ago as a way of stabilizing PaCO2 in hypercapnic patients using either positive pressure (1), negative pressure (...

The use of capnometry to predict arterial partial pressure of CO(2) in non-intubated breathless patients in the emergency department.

BackgroundCapnometry measures carbon dioxide in expired air and provides the clinician with a noninvasive measure of the systemic metabolism, circulation and ventilation. This study was carried out on patients with acute breathlessness to define the utility and role of capnometry in the emergency department.AimThe objectives of the study were: To determine the correlation between end tidal CO2 and PaCO2 in non-intubated acutely breathless patients.To determine factors that influence the end tidal carbon dioxide (ETCO2).To determine the correlation between ETCO2 with PaCO2 in patients presenting with pulmonary disorders. MethodsOne hundred fifty acutely breathless patients arriving at the emergency department and fulfilling the inclusion and exclusion criteria were chosen during a 6-month study period. The patients gave written or verbal consent, and were triaged and treated according to their presenting complaints. Demographic data were collected, and the ETCO2 data were recorded. Arterial blood gas was taken in all patients. The data were compiled and analyzed using various descriptive studies from the Statistics Program for Social Studies (SPSS) version 12. Correlation between ETCO2 and PaCO2 was analyzed using the Pearson correlation coefficient. Other variables also were analyzed to determine the correlation using simple linear regression. The agreement and difference between ETCO2 and PaCO2 were analyzed using paired sample t-tests.ResultsThere is a strong correlation between ETCO2 and PaCO2 using the Pearson correlation coefficient: 0.716 and p value of 0.00 (p < 0.05). However, the paired t-test showed a mean difference between the two parameters of 4.303 with a p value < 0.05 (95% CI 2.818, 5.878). There was also a good correlation between ETCO2 and acidosis state with a Pearson correlation coefficient of 0.374 and p value 0.02 (p < 0.05). A strong correlation was also observed between ETCO2 and a hypocapnic state, with a Pearson correlation coefficient of 0.738 (p < 0.05). Weak correlation was observed between alkalosis and ETCO2, with a Pearson correlation coefficient of 0.171 (p < 0.05). A strong negative correlation was present between ETCO2 and hypercapnic patients presenting with pulmonary disorders, with a Pearson correlation coefficient of -0.738 (p < 0.05) and of -0.336 (p < 0.05), respectively.ConclusionThis study shows that ETCO2 can be used to predict the PaCO2 level when the difference between the PaCO2 and ETCO2 is between 2 to 6 mmHg, especially in cases of pure acidosis and hypocapnia. Using ETCO2 to predict PaCO2 should be done with caution, especially in cases that involve pulmonary disorders and acid-base imbalance.

S67 Phenotypic differences between obese patients with eucapnic and hypercapnic sleep-disordered breathing (SDB)

BackgroundObesity-related SDB requiring domiciliary non-invasive ventilation (NIV) can present as (1) eucapnic obstructive sleep apnoea (OSA) (2) hypercapnic OSA (PaCO2 >6 kPa) (3) hypercapnic OSA with obesity hypoventilation syndrome (OHS)...

S66 A randomised crossover trial of pressure support ventilation (PSV) versus pressure controlled ventilation (PCV) in stable hypercapnic Chronic Obstructive Pulmonary Disease (COPD)

IntroductionPSV, rather than PCV, is often the preferred mode of ventilatory support in stable hypercapnic COPD patients, although this is supported by limited data. We hypothesised that PCV would be...

P158 The strength of association between the risk of endotracheal intubation and initial arterial blood (ABG) pH in patients presenting with acute hypercapnic respiratory failure (AHRF) treated with non-invasive ventilation (NIV)

IntroductionThe risk of failure of non-invasive ventilation (NIV) in AHRF patients is greater with higher degrees of acidosis. The BTS guidelines suggest that patients with pH <7.26 have a higher...

Predicting Nocturnal Hypoventilation in Hypercapnic Chronic Obstructive Pulmonary Disease Patients Undergoing Long-Term Oxygen Therapy

Background: Chronic obstructive pulmonary disease (COPD) patients are very sensitive to changes in pulmonary mechanics and central ventilation control during sleep and may develop significant gas exchange alterations with increased hypoxemia and hypercapnia. Oxygen therapy improves nocturnal desaturation but can worsen hypoventilation. Objectives: To analyze the prevalence of nocturnal hypoventilation (NHV) in hypercapnic COPD patients and to determine predictive factors for this phenomenon. Methods: This was a prospective multicenter study which enrolled 80 clinically stable COPD patients with hypercapnic respiratory failure who fulfilled the conventional criteria for long-term oxygen therapy (LTOT). All patients had undergone pulmonary function testing, blood gas analysis, and respiratory polygraphy. Arterial blood gas samples were obtained while patients were awake and during sleep. NHV was considered when an increase in PaCO₂ >10 mm Hg was observed in any nocturnal arterial blood gas sample as compared to the awake levels. Results: Seventeen patients (21%) developed NHV. NHV was associated with the values of BMI, hemoglobin, hematocrits, DLCO, and PaO₂ reached after oxygen administration. In the logistic regression analysis BMI (OR 1.26, 95% CI 1.068–1.481; p = 0.006) and the diurnal increase of PaO₂ after O₂ (OR 0.89, 95% CI 0.807–0.972; p = 0.010) were the variables that best discriminated with a sensitivity of 82% and a specificity of 78%. Conclusions: NHV is a relatively common finding in stable hypercapnic COPD patients undergoing LTOT and it is related to a higher BMI and lower PaO₂ after oxygen administration.

Pros and cons of permissive hypercapnia in patients with subarachnoid haemorrhage and ARDS

Petridis and colleagues describe their results of intracranial pressure (ICP) analysis in 12 patients after subarachnoid haemorrhage (SAH) treated with permissive hypercapnia due to acute respiratory distress syndrome (ARDS) [6]. The study is of interest for physicians practicing neurosurgical intensive care, since many patients who suffer from severe SAH develop serious pulmonary problems during their stay in the intensive care unit. In general, these patients have a very high mortality rate and, therefore, the authors have to be congratulated on their good results. However, there are several aspects of the paper which should compel the reader to interpret the results very carefully: On the one hand, the regimen described is in contrast to the widely accepted opinion that hypercapnia should be avoided in brain-damaged patients, since hypercarbia potentially leads via acidosis-induced cerebral vasodilatation to an increase of intracranial blood volume which again leads to an increase of ICP [1–3, 5, 7]. Therefore, patients with elevated ICP have notably been excluded from studies on permissive hypercapnia [1]. Also other side effects of hypercarbia—especially severe acidosis with its deleterious effects in intensive care medicine— have to be kept in mind. On the other hand, there are animal studies demonstrating a beneficial effect of hypercapnia on the central nervous system: Zhou and colleagues concluded in their recently published paper that mild to moderate hypercapnia is neuroprotective after transient global cerebral ischemia–reperfusion injury, whereas severe hypercapnia increased brain injury [8]. Hare and colleagues hypothesized in their paper that the combined effect of increased cerebral blood flow, PaO2, and reduced pH collectively contribute to augmenting cerebral tissue oxygen tension during hypercapnia [4]. Thus, at present a generally accepted recommendation about permissive hypercapnia in brain injured patients cannot be given. In my opinion, permissive hypercapnia should to date only be administered in patients with a therapy refractory ARDS in whom advanced methods to reduce hypercarbia—e.g., jet ventilation or interventional lung assist devices—if available—have not been successful, i.e., as a form of an individual treatment attempt. A continuously performed ICP monitoring seems to be mandatory—as performed by the authors in the paper [6]. Furthermore, it has to be pointed out that there are some methodological weaknesses of the paper [6]: This is not a controlled randomized clinical study, but the report of a retrospective observation of non-consecutive patients. Another important point is that ICP measurements have been performed while the external ventricular drainage (EVD) was still open: Thus, it is unclear whether hypercapniainduced intracranial vasodilatation has not been compensated by an increase of CSF outflow via the EVD. As a conclusion, the treatment reported in the paper by Petridis and colleagues [6]—even if there are really interesting aspects, especially the potentially neuroprotective role of mild to moderate hypercapnia [8]—cannot generally be recommended until studies with a better design, especially controlled, randomized studies, have confirmed the results.

Effect of different levels of pressure support on physiological variables and patient-ventilator synchronicity during noninvasive pressure support ventilation in patients with respiratory failure

To evaluate the effects of different levels of pressure support (PS) during noninvasive pressure support ventilation (NPPV) on physiological variables, patient-ventilator synchronicity in patients with acute exacerbation chronic obstructive pulmonary disease (AECOPD) and hypercapnic respiratory failure. Fifteen hypercapnic respiratory failure AECOPD patients requiring NPPV in respiratory intensive care unit (RICU) were enrolled. Three different PS levels of 5, 10, 15 cm H2O (1 cm H2O=0.098 kPa) were applied randomly in all the 15 patients. At each PS level the patient was ventilated for 30 minutes, whereas physiological variables, ineffective effort (IE) expressed as IE index were recorded within the last 2 minutes. The IE index, tidal volume (VT), minute ventilation (VE), coefficient of variation of VT, ventilator inspiratory time (TI), expiratory time (TE), leak volume at 15 cm H2O PS level were significantly higher than those at 5 cm H2O level [IE index: (33.8+/-9.1)% vs. (8.0+/-6.0)%, VT (ml): 626+/-203 vs. 339+/-115, VE (L/min): 11.1+/-4.7 vs. 7.7+/-2.7, coefficient of variation of VT: (32.6+/-15.5)% vs. (11.3+/-6.9)%, TI (s): 1.14+/-0.31 vs. 0.76+/-0.15, TE (s): 2.49+/-0.44 vs. 1.87+/-0.28, leak volume (L/min): 8.28+/-4.86 vs. 2.22+/-1.58, all P<0.05], while the ventilator respiratory rate [(17+/-3) breaths/min] was lower at 15 cm H2O PS level than that at 5 cm H2O level [(23+/-3) breaths/min, P<0.05]. At 5 cm H2O level, the IE index was positively correlated with TI (r=0.62, P<0.05). Furthermore, the increase in IE index followed by PS level increase was correlated negatively with the change of VT (Delta VT) and positively with that of the TI (Delta TI, R2=0.88, P=0.000). (1) The IE at low assistance is associated with prolonged TI. (2) High PS level can significantly increase VE and VT, and reduce the ventilator respiratory rate. However, high PS level also lead to higher IE than low level. The factors favoring a higher increase in IE index as PS level increased include a less increase in VT and a higher increase in TI. However, an increase in leak volume is not associated with an elevated incidence of IE. (3) IE is high at high PS level during NPPV, even the Shape-signal is used as a trigger mechanism.

Noninvasive ventilation after extubation reduced respiratory failure and 90-day mortality in hypercapnic patients

Source Citation Ferrer M, Sellares J, Valencia M, et al. Non-invasive ventilation after extubation in hypercapnic patients with chronic respiratory disorders: randomised controlled trial. Lancet. 2...

Poor sleep quality is associated with late noninvasive ventilation failure in patients with acute hypercapnic respiratory failure*

To determine whether sleep quality helps to predict noninvasive ventilation outcome in patients with acute hypercapnic respiratory failure. Despite an initial clinical improvement, nearly one fourth of patients may fail noninvasive ventilation after several days. Because late intubation is associated with a poor prognosis, it may be useful to identify factors that may predict or explain late noninvasive ventilation failure. We prospectively studied 27 hypercapnic patients in a medical intensive care unit who required noninvasive ventilation for >48 hrs. A 17-hr sleep polysomnography (3 PM-8 AM) was recorded 2 days to 4 days after noninvasive ventilation initiation. Late noninvasive ventilation failure was defined as death, endotracheal intubation, or persistent need for noninvasive ventilation on day 6. An abnormal electroencephalographic pattern that eluded analysis by standard sleep-scoring criteria was noted in seven (50%) of the 14 patients with late noninvasive ventilation failure compared with one (8%) of the 13 patients successfully treated with noninvasive ventilation (p = .03). No clinical or laboratory variables explained the electroencephalographic differences. Patients failing noninvasive ventilation had poorer sleep quality with greater circadian sleep-cycle disruption and less nocturnal rapid eye movement sleep (6 mins [range, 0-12] vs. 26 mins [range, 6-49], p = .03), compared with patients successfully treated with noninvasive ventilation. Noninvasive ventilation failure was associated with delirium during the intensive care unit stay (64% vs. 0%). Late noninvasive ventilation failure in elderly patients with acute hypercapnic respiratory failure was associated with early sleep disturbances including an abnormal electroencephalographic pattern, disruption of the circadian sleep cycle, and decreased rapid eye movement sleep.

Sleep hypoventilation due to increased nocturnal oxygen flow in hypercapnic COPD patients

This study shows the risks and benefits of increasing the nocturnal oxygen flow in hypercapnic COPD patients undergoing LTOT, as recommended by some COPD treatment guidelines to avoid nocturnal desaturation. Several COPD treatment guidelines recommend increasing oxygen flow during sleep to avoid nocturnal desaturation. However, such an increase could have deleterious clinical and gas exchange effects. The objective of this study was to evaluate short-term gas exchange alterations produced by increasing the nocturnal oxygen flow rate. Thirty-eight COPD patients with chronic hypercapnic respiratory failure were evaluated. In a cross-over study, patients were randomly assigned to receive the daytime oxygen flow rate on one night and an additional litre on the alternate night. Nocturnal pulse oximetry and arterial blood gases at awakening were measured, in each patient, on two consecutive days. The administration of 1 L more oxygen during the night resulted in improved parameters of nocturnal oxygenation (oxygen pulse oximetry saturation-SpO2; percentage of sleep time spent at SpO2<90%-CT90; PaO2 at awakening). Nevertheless, such an increase in oxygen flow during the night was also associated with greater hypercapnia and acidosis (p<0.05) the next morning. The increase of oxygen flow in severe COPD patients with established daytime hypercapnia improved nocturnal oxygenation but it also led to greater hypercapnia and respiratory acidosis at awakening in a considerable proportion of these patients.