The mortality of CDH when complete case ascertainment is achieved is unaffected by new therapies. The survival rate is principally determined by the rate of antenatal termination and the incidence of associated anomalies. Reports of improved survival of CDH should be interpreted with caution, as variations in outcome are more likely to be explained by case selection artifact.
The quality of sleep is significantly compromised in many patients with chronic obstructive pulmonary disease (COPD) and may be further diminished when certain comorbidities are present. A reduced sleep quality is associated with daytime consequences like fatigue, psychiatric problems and an impaired quality of life. Sleep induces physiologic alterations in respiratory function, which can become pathologic and may provoke or worsen hypoxemia and hypercapnia in COPD. Dyspnea, cough and excessive mucus production should be optimised to minimise causes for sleep disturbance. Pharmacological therapy may be helpful; sedatives like benzodiazepines and non-benzodiazepine benzodiazepine-receptor agonists (NBBRAs) are (equally) effective in improving sleep quality. Whether or not these hypnotics produce serious adverse respiratory effects during sleep, remains unclear due to opposing studies. Therefore, their use should be as short as possible.
Background: Measurements of transcutaneous carbon dioxide tension (PtcCO2) with current devices are proven to provide clinically acceptable agreement with measurements of partial arterial carbon dioxide tension (PaCO2) in several settings but not during cardiopulmonary exercise testing (CPET). Objectives: The primary objective of this study was to investigate the agreement between PaCO2 and PtcCO2 measurements (using a Tosca 500 with a Tosca sensor 92) during CPET. A secondary objective was to investigate the agreement between arterial and transcutaneous oxygen saturation (SaO2, SpO2) as measured with this sensor during CPET. Methods: In patients with various pulmonary diseases, PtcCO2 and SpO2 were continuously measured and compared with arterial blood gas samples during CPET. A maximum bias of 0.5 kPa and 95% limits of agreement (LOA) of 1 kPa between carbon dioxide pressure (PCO2) measurements were determined as clinically acceptable. Results: In total 101 ‘paired’ arterial and transcutaneous measurements were obtained from 21 patients. Bias between PaCO2 and PtcCO2 was –0.03 kPa with LOA from –0.78 to 0.71 kPa. Bias between SaO2 and SpO2 was –1.0% with LOA from –2.83 to 0.83%. Conclusions: Transcutaneous estimations of PCO2 and SpO2 are accurate and can be used in CPET, circumvening the need for arterial cannulation.
One week usage of temazepam 10mg does not influence circadian respiratory function, dyspnea, and sleepiness in patients with stable, severe, normocapnic COPD and insomnia and it improves total sleep time and subjective sleep latency. However, this is a preliminary explorative study for assessing the feasibility to perform a larger study on this topic. The clinical implications of this study are very limited.
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