Activity of dorsal medullary respiratory neurons in awake rats.
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Biomedical subjects
Publications and source records attributed to W McNicholas.
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Respiratory sinus arrhythmia (RSA) is the variation of heart rate (or RR interval) in phase with respiration and has been extensively studied. However, the effect of respiration on atrioventricular conduction delay (and hence PR interval length) has not yet received much attention. This work reports on measurements of respiration and associated RR and PR variability, in 11 subjects, assessed through surface electrocardiogram measurements, for both paced and spontaneous respiration in the supine position. A wavelet-based approach was used to extract RR and PR intervals. The accuracy of RR and PR interval measurement was consistent with previously published work. Respiratory atrioventricular conduction delay variability (RCV) was assessed using three techniques: spectral, peak-to-trough and cosinor methods. All measures showed statistically significant variations in PR interval due to respiration during paced respiration at 6 min(-1). Of the three measures, cosinor analysis was most reliable in highlighting RCV. Using this measure, statistically significant RCV was seen in ten out of the 11 subjects during paced respiration. The magnitude of the variability was estimated as +/- 5.9% of the mean PR interval. In spontaneous respiration, statistically significant RCV was seen in approximately half of the subjects, with an estimated variability of +/- 1.5%. As a control, statistically significant values for RSA were also obtained from the same data, which agreed with previously published measurements. It was concluded that respiration does indeed modulate atrioventricular conduction delay, deep breathing in the supine position accentuates this effect, and cosinor analysis provides a reliable means for quantifying this effect.
Cytomegalovirus (CMV) pneumonia in the setting of non-transplantation patients is a rarity. We present a case of CMV pneumonitis in a woman with stage IV breast cancer, with brain metastases, receiving both chemotherapy and systemic corticosteroids. A review of the literature reveals this as a unique case. Potential viral etiologies should therefore be considered in cancer patients with pneumonia receiving non-transplantation chemotherapy-regimens, particularly if steroids are a component of their therapy.
The modest antitumor activity and clinical benefit of conventional platinum-containing multidrug regimens in locally advanced and metastatic non-small cell lung cancer have provided the impetus for the development of novel combinations. The promising single-agent activity of docetaxel makes it an obvious candidate for incorporation into active programs. The Irish Clinical Oncology Research Group is conducting a phase I-II evaluation of a three-drug combination of docetaxel, ifosfamide, and cisplatin with lenograstim support in patients with stages III-IV non-small cell lung cancer. Preliminary results indicate that the regimen is feasible and tolerable up to a maximum tolerated dose level of 3,000 mg/m2 ifosfamide, 75 mg/m2 cisplatin, and 75 mg/ m2 docetaxel. The regimen appears to be quite active, with nine of 12 evaluable patients responding in the phase I component of the trial. This dose level is currently being explored in a phase II trial.
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A 30-year-old female patient presented in a comatose state with clinical and radiographic signs of aspiration pneumonia 16 hours following elective surgery. Subsequent clinical assessment and investigations revealed the characteristic facies, proximal muscle weakness, lenticular opacities, pulmonary function defects, arterial desaturation and abnormal breathing during rapid eye movement (REM) sleep often associated with myotonia dystrophica. Although these characteristic features were evident on clinical examination postoperatively they were not noted in the preoperative assessment. The aspiration pneumonia and coma were unusual presenting features of this disease. Unsuspected myotonia dystrophica should be considered in the differential diagnosis of unexplained respiratory depression, aspiration or comatose state following surgery. Recognition of the disorder during the preoperative assessment is the key to avoiding complications during the perioperative management of such patients.
Fundamental to the pathogenesis of obstructive sleep apnea (OSA) is the interaction of physiologic and anatomic alterations of the upper airway. However, many patients with OSA have no identifiable abnormality of the upper airway, and they have been termed idiopathic. In an attempt to find a structural deviation in upper airway anatomy, we performed acoustic echography and cephalometric roentgenograms in 9 male patients with OSA and no clinical evidence of upper airway abnormality. Mean cross-sectional area of the pharynx by acoustic reflection was less in these patients (3.7 +/- 0.8 cm2) than in subjects in a control group (5.3 +/- 0.6 cm2) (p less than 0.001). Mean glottic cross-sectional area was less in the patient group (1.5 +/- 0.5 cm2) than in the control group (2.7 +/- 0.5) (p less than 0.001). There was a significant correlation between the number of apneas per sleep hour and pharyngeal cross-sectional area (r = 0.87, p less than 0.01). Cephalometric analysis indicated that the patients had smaller mandibles by a mean of 5.4 +/- 6.6 mm (p less than 0.05). The overall posterior displacement of the mandibular symphysis, which is representative of the skeletal support of the anterior pharyngeal wall and is dependent on both mandibular size and position, was highly significant (6.4 +/- 4.7 mm) (p less than 0.01). Furthermore, there was a significant correlation between the number of apnea episodes per sleep hour and the total posterior displacement (r = 0.67, p less than 0.05). This study indicates that patients with so-called idiopathic OSA may have an anatomic predisposition to the development of upper airway occlusion that may not be detectable on clinical examination.
A 67-yr-old man presented with a 4-yr history of chronic ventilatory failure in the absence of any restrictive or obstructive ventilatory defect. Detailed neurologic investigations were unremarkable, and the response of minute volume of ventilation to inhaled CO2 was normal. During sleep there was no evidence of upper airway obstruction, and minute volume of ventilation averaged 6.7 L/min, compared with 7.2 L/min during quiet wakefulness. However, sleep was associated with a rapid and shallow pattern of breathing, resulting in high dead space ventilation, inadequate alveolar ventilation, hypoxemia, and hypercapnia. Correction of the abnormal ventilatory pattern during sleep by diaphragmatic pacing abolished all features of chronic respiratory failure. The findings indicate that a disorder of respiratory pattern during sleep can produce chronic ventilatory failure, despite normal respiratory drive.