We observed multiple significant correlations between indices of sleep quality and daytime PFTs in a group of healthy older persons, particularly those with low sleep efficiency. These relationships between variations in sleep quality and PFTs represent an extension of earlier research demonstrating that sleep deprivation results in worsened pulmonary function the following day. The present results are correlational, so we cannot state with certainty that sleep quality affects pulmonary function rather than vice versa; however, previous work indicates that decrements in pulmonary function following sleep loss are reversible with sleep restoration. …Read the rest of this article
Category: Pulmonary Function
A total of 48 subjects met criteria for inclusion in the study. The mean age of our subjects was 69.6 years (range, 60 to 87 years). There were 21 women and 27 men. Sleep quality variables are reported in Table 1; mean pulmonary function data are reported in Table 2. Good sleepers had significantly greater FEV/FVC ratios than did poor sleepers.
The initial data analysis of the entire group of subjects is presented in Table 3. Time in bed correlated positively with MW, the number of movements related negatively to FEV/FVC and MW, and the percentage of stage 0 sleep (awake) correlated negatively with FVC (percent predicted) and FEVi (percent predicted). There were no relationships indicating that poor or disturbed sleep positively correlated with pulmonary function. …Read the rest of this article
In order to index sleep disturbance, we chose several measurements reported to reflect sleep quality in older persons, including the following: total sleep time; sleep efficiency (time asleep/time in bed); number of body movement artifacts; and the percentage of sleep time spent in stages 0, 1, 2, 3, and 4, and REM sleep. We calculated measurement of sleep-disordered breathing (apnea-plus-hypopnea index; mean low Sa02; number of nocturnal desaturations of >4 percent) using a modification of a scoring system previously described. …Read the rest of this article
“Lights-out” was as close to 11:00 pm as possible, with wake up at 6:00 or 6:30 am; however, as we were trying to emulate routines that subjects followed at home, they were allowed out of bed to go to the bathroom or to turn on the light to read, if they desired.
Apparatus included a Grass (model 78) polygraph for one laboratory and a Nihon-Khoden (model EEG 4123P) polygraph for the other. Sleep was measured through a standard coronal montage using the International 10/20 system with electrode placement at C3, C4, C„ Oi, 02, electro-oculogram, and chin electromyogram. Electrocardiograms were recorded from a standard one-lead montage. …Read the rest of this article
Loss of sleep results in deterioration of pulmonary function in normal humans and causes modest worsening of pulmonary function in patients with moderate chronic obstructive pulmonary disease. Since gross sleep disturbances cause worsening of routine PFTs, we wondered if more subtle variations in sleep quality and pulmonary function might be related in normal humans. To investigate this question, we chose to study a population which is known to experience a wide variation in sleep architecture, the healthy elderly. The purpose of our study, then, was to investigate the relationship between sleep quality and performance of PFTs in healthy people over 60 years of age. add comment
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Comment: This diabetic woman presented with P mira-bilis bacteremia and an exudative pleural effusion infected with three organisms including Proteus. The enterococci and diphtheroids might have been contaminants. After an extensive and unsuccessful search for pneumonia, neurologic signs and symptoms led to the diagnosis of vertebral osteomyelitis caused by P mirahilis. The delay of 42 days before the diagnosis of osteomyelitis probably contributed to the neurologic complication.
A 62-year-old man with diabetes mellitus and coronaiy artery disease had gradual onset of back pain and a mild productive cough for 3 months. There was no history of shortness of breath, chest pain, fever, or weight loss. Breath sounds were decreased over the right lung and the WBC count was 26,000/μL. A right-sided pleural effusion was seen on a chest x-ray film, and a CT scan of the thorax confirmed a loculated effusion. The pleural fluid was sterile but exudative (protein level, 4.2 g/dL; LDH value, 513 U/L) so antibiotics online. The serum protein and LDH levels were 4.9 g/dL and 160 IU/L, respectively. Blood cultures grew Streptococcus agalactiae. He was treated with IV ceftazidime and was discharged home on a regimen of oral penicillin after a 9-day hospital stay. He continued to have fever and was readmitted 20 days later. Thoracentesis yielded a sterile exudative pleural effusion. Because of persistence of the effusion, despite 2 weeks of antibiotic therapy, the patient required chest tube drainage and thoracotomy and decortication subsequently. On the 22nd hospital day, tenderness in the region of the 6th and 7th thoracic vertebrae was noted. An MRI showed destruction of the inferior plate of the 6th and the superior plate of the 7th thoracic vertebrae consistent with a disk space infection and vertebral osteomyelitis (Fig 3). The patient was treated with IV clindamycin for 8 weeks, which resulted in clinical improvement, and the pleural effusion resolved. The patient has been followed up for 4 years, and he has not had any recurrence of the effusion.
Comment: This diabetic man presented with pleural effusion associated with S agalactiae bacteremia. The delay in diagnosis of osteomyelitis was 42 days. The thoracotomy and decortication may have been avoided if the diagnosis had been made earlier. It was only after prolonged IV clindamycin therapy that the patient improved.
Figure 3. MRI of the spine (of case 3) showing increased signal intensity in the disk space on T-2- weighted image suggestive of disk infection. There is destruction of the vertebral body of T6-7.
Our study did not investigate the mechanisms of action of NMV in our patients. We can postulate that these mechanisms do not appear to be different from those proposed in other etiologies of respiratory failure: improvement in alveolar ventilation and distribution of ventilation, rest of the respiratory muscles, and resetting of the respiratoiy drives. If we consider, in our series, the lack of improvement of PaC02, the improvement in alveolar ventilation was difficult to confirm; however, if we consider the lack of worsening of PaC02 despite the use of higher FIo2, as described above, improvement of alveolar ventilation or of V/Q inequalities is plausible. An improvement in the quality of bronchial drainage, promoted by intermittent positive pressure ventilation, may play a role in clinical improvement in patients with bronchiectasis. This may also explain the lower incidence of respiratoiy tract infection in our patients. Long-term efficacy also depends on long-term tolerance and compliance to the apparatus. In this instance, our positive results are probably partially due to the close attention paid to patient comfort (choice of different models of masks, no use of contention to close mouth).
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