Ventilatory response to hypoxia in experimental pathology of the diaphragm.

In this study, we examined the usefulness of arterial blood gas variables, as changed by the hypoxic stimulus, in discerning various experimentally-induced conditions of diaphragm weakness in anesthetized cats. We defined three experimental situations (models): (i) intact muscle, statistical Class I, (ii) four degrees of muscle dysfunction (after sequential diaphragm denervation), Classes II-V, and (iii) entirely paralyzed muscle, Class VI. Responses to a hypoxic stimulus in the above-mentioned conditions were evaluated by using the methods of the pattern recognition theory. We found that before the hypoxic stimulus, with partial but of different severity denervation of the diaphragm, the k-nearest neighbor classifier (k-NN) assigned 100% of the classified cases to Class II (one phrenic nerve rootlet cut). In contrast, during hypoxia only 67% of cases were assigned to Class II, the remaining being spread throughout other classes of muscle weakness. When one limits the procedure to the extreme classes: Class I (intact diaphragm) and Class VI (totally denervated diaphragm), the k-NN picks out 33% and 50% cases of bilateral diaphragm paralysis before and during hypoxia, respectively. We conclude that any remaining innervations of the diaphragm ensure the functionally optimal level of lung ventilation that may waver when hypoxia develops.

[Effect of halothane on ventilation and arterial blood gases in rats with and without diaphragmatic paralysis]. / Effets de l'halothane sur la ventilation et les gaz du sang arteriel chez le rat avec ou sans paralysie diaphragmatique.

Some patients with diaphragmatic paralysis or dysfunction maintain ventilation by use of other muscles. Anaesthesia, in modifying the performance of these muscles, presents a potential risk to such patients. To evaluate this risk, the effects of halothane on ventilation and arterial blood gases were studied on a model of bilateral diaphragmatic paralysis, the phrenectomized rat. The study was performed on 43 rats. Success of phrenectomy was confirmed at laparotomy, which did not result in blood gas changes. Laparotomy was performed in 23 rats and a carotid artery was catheterized. In 11 control rats, phrenic nerves were exposed but not sectioned, and in 12 other rats, the phrenic nerves were sectioned. Ventilation was measured by plethysmography in awake rats before and after surgery and in the same rats anaesthetized with halothane 1.1%. In the 23 rats, a decrease in weight and core temperature was observed after operation and this was more marked in phrenectomized than in control rats. In the 11 control rats, ventilation increased postoperatively without change in blood gases. In these rats, halothane caused a decrease in minute ventilation and PaO2 and an increase in PaCO2. Phrenectomy in awake rats led to an increase in minute ventilation, hypoxaemia and hypercapnia. In these rats, halothane led to death in three and a decrease in minute ventilation, with hypercapnia and hypoxaemia in the nine other rats. Blood gas changes were greater than in anaesthetized controls. In the intact rat, halothane leads to blood gas changes comparable to those observed in other species and humans. The present study confirms the effects of halothane on respiratory muscles other than the diaphragm and demonstrates the severe respiratory risk of anaesthesia in patients whose ventilation is maintained by these muscles.

Arterial oxygen saturation and posture in acute stroke.

Patients with acute stroke are at risk of hypoxaemia and the degree of oxygen desaturation may depend on posture. Using a fingertip pulse oximeter, we studied the effects of different nursing positions on arterial oxygen saturation (SaO2) in ten elderly patients within 48 hours of a hemiplegic stroke and 10 age-matched controls admitted to hospital with other acute illnesses. Mean SaO2 was consistently higher in the controls than the stroke patients in all recumbent positions, but when patients were propped up the difference between the groups was statistically insignificant. The difference between semirecumbent and lying SaO2 values was then tested in a further nine stroke patients. Overall the mean SaO2 was significantly higher and, in at least four cases, the duration of episodes of desaturation (SaO2 < 90%) was substantially less when the patients were propped up. We suggest that, wherever possible, acute stroke patients should be nursed sitting up to minimize the risk of oxygen desaturation and possible aggravation of ischaemic brain damage.

Obstructive sleep apnea complicating negative-pressure ventilatory support in patients with chronic paralytic/restrictive ventilatory dysfunction.

The purpose of this study was to determine the incidence and severity of obstructive events and oxyhemoglobin desaturation (dSaO2) in 37 patients with paralytic/restrictive ventilatory insufficiency during use of nocturnal ventilatory assistance provided by means of negative-pressure body ventilators (BVs). Thirteen of the 37 patients had mean oxyhemoglobin saturation (SaO2) less than 95 percent and a mean of ten or more episodes per hour when the dSaO2 was greater than or equal to 4 percent (4%dSaO2/h). In all, 26 of the 37 patients had evidence of significant multiple episodes of dSaO2 while asleep on BVs. Polysomnography performed on three of these patients substantiated the obstructive nature of the dSaO2. Twenty-two of the 37 patients who had a mean SaO2 of 90.6 +/- 7.2 percent and a mean of 17.7 +/- 16.1 4%dSaO2/h on BVs were switched to noninvasive ventilatory assistance by intermittent positive airway pressure (NV-PAP). Their mean SaO2 improved to 96.0 +/- 2.2 percent, and the 4%dSaO2/h decreased to 1.2 +/- 1.8 per hour. All symptoms similar to those of obstructive sleep apnea were relieved. We conclude that BV use is associated with significant dSaO2 in over 50 percent of patients. The dSaO2 is predominantly obstructive in nature but may be due to chronic underventilation in patients using less effective BVs. Patients with a mean SaO2 less than 95 percent or 10 or more 4%dSaO2/h may benefit from conversion to NV-PAP via the nose, the mouth, or an oral-nasal interface.

Diaphragmatic plication for unilateral diaphragmatic paralysis: a 10-year experience.

Unilateral paralysis of the diaphragm due to nonmalignant disease is an uncommon disorder previously thought to have benign implications. Some patients, however, experience dyspnea and orthopnea with impairment of pulmonary function. Unilateral diaphragmatic plication was performed on 17 patients (16 men and 1 woman with a mean age of 53.7 years [range, 28 to 74 years]) during the last 10 years. Preoperatively each patient was shown to have paradoxical movement of the paralyzed diaphragm on sniffing and to have a reduction in forced vital capacity and lung volumes. These reductions were greater when the patient was in the supine position. All patients had moderate hypoxemia (mean arterial oxygen tension, 73.1 +/- 10.9 mm Hg). Plication was performed by imbricating the diaphragm in layers through a thoracotomy incision. After plication, all patients showed both subjective and objective improvement. Six patients were reassessed 5 or more years after plication (range, 5 to 7 years), and the improvement was maintained. Diaphragmatic plication is a safe and effective procedure for adult patients with dyspnea due to unilateral diaphragmatic paralysis; furthermore, the initial improvement is maintained.

Sudden infant death syndrome. The role of putrefactive toxins in respiratory paralysis and cerebral coma.

The Sudden Infant Death Syndrome (SIDS) is responsible for the death of 10,000 infants annually in the U.S.A. The cause of these deaths is not known; all SIDS infants studied died during sleep in a silent fashion and there are no specific lesions observable post mortem. It may be of significance, however, that nearly half of SIDS infants had a respiratory tract infection in the last two weeks of life while forty percent had bloody froth over their mouths when found, presumably pulmonary oedema fluid. It is hypothesis that improper feeding or diarrhoea may likewise be involved in SIDS and that enterotoxins from putrefactive products are the precipitating event in this syndrome.

Effect of cervical spinal cord hemisection and hemidiaphragm paralysis on arterial blood gases, pH, and respiratory rate in the adult rat.

We documented the changes that occur in arterial blood gases, pH, and respiratory rate in rats subjected to a C2 spinal cord hemisection which results in paralysis of the ipsilateral hemidiaphragm. The results indicated that rats compensate for hemidiaphragm paralysis by maintaining arterial pO2 through an increased rate of respiration. This observation is of interest because it implies a form of functional recovery from spinal cord injury which has heretofore not been demonstrated.