Hypoventilation

About: Hypoventilation is a research topic. Over the lifetime, 1772 publications have been published within this topic receiving 40799 citations. The topic is also known as: respiratory depression.

Loss of catecholaminergic neurons in the medullary reticular formation in myotonic dystrophy

Abstract: Objective: To clarify the possible relation between the extent of involvement of catecholaminergic neurons and the presence of alveolar hypoventilation in patients with myotonic dystrophy (MyD). Background: Respiratory insufficiency has been reported frequently in MyD patients. Recent data support the hypothesis that this respiratory failure results from a primary dysfunction of the CNS. Methods: The authors performed a quantitative immunoreactive study of tyrosine hydroxylase immunoreactive (TH+) neurons linked to hypoventilation in the dorsal central medullary nucleus (DCMN), the ventral central medullary nucleus (VCMN), and the subtrigeminal medullary nucleus (SMN)-where the automatic respiratory center is thought to be located-in eight MyD patients and in 10 age-matched control subjects. Alveolar hypoventilation of the central type was present in three of the MyD patients but not in the remaining MyD patients or the control subjects. Results: The densities of TH+ neurons of the DCMN, the VCMN, and the SMN in MyD patients with hypoventilation were significantly lower than in those without hypoventilation ( p p p p p p Conclusions: These data suggest that the loss of TH+ neurons of the DCMN, the VCMN, and the SMN is associated with the presence of hypoventilation in MyD and may be an important feature of MyD.

Primary Alveolar Hypoventilation Associated with Western Equine Encephalitis

Abstract: Excerpt The alveolar hypoventilation syndrome, characterized by arterial hypercapnia, develops when alveolar ventilation falls below a critical value. Fishman, Turino, and Bergofsky reviewed the cl...

Management alternatives for post-polio respiratory insufficiency. Assisted ventilation by nasal or oral-nasal interface.

Abstract: Post-poliomyelitis patients may develop insidious respiratory failure. Chronic alveolar hypoventilation symptoms are often misdiagnosed and the condition is frequently treated inappropriately by oxygen therapy. Physicians are often at a loss to offer assisted ventilation by noninvasive methods and tracheostomy and long-term tracheostomy intermittent positive pressure ventilation is often refused. We studied the use of two noninvasive positive airway pressure alternatives for the nocturnal ventilatory support of 31 post-poliomyelitis patients. These methods were intermittent positive pressure ventilation via nasal access (NIPPV) and via a strapless oral-nasal interface (SONI IPPV). The use of custom fabricated interfaces was also evaluated. Practical alternatives for assisted daytime ventilation included glossopharyngeal breathing, the pneumobelt ventilator and mouth intermittent positive pressure ventilation. Overnight sleep monitoring was performed on 10 patients breathing autonomously or with body ventilators then repeated on NIPPV and/or SONI IPPV. The mean sleep oxygen saturation (SaO2) increased from 87.5 +/- 9.1% on unassisted breathing or body ventilators to 96.2 +/- 2.0% (P less than 0.01) on NIPPV or SONI IPPV. Of 12 other patients with a mean vital capacity of 472 +/- 480 ml and no significant free time supine, 11 patients also maintained SaO2 greater than 94% during sleep supine on NIPPV and/or SONI IPPV. Twenty-one patients have been on nocturnal NIPPV for an average of 23 (3-70) months. Six have been on nocturnal SONI IPPV for an average of 35 (5-66) months. All patients' hypoventilation symptoms were relieved. In conclusion, NIPPV and SONI IPPV can improve the nocturnal ventilation of post-poliomyelitis patients with chronic alveolar hypoventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of aminophylline on the threshold for initiating ventricular fibrillation during respiratory failure.

Abstract: Cardiac arrhythmias have frequently been reported in association with respiratory failure. The possible additive role of pharmacologic agents in precipitating cardiac disturbances in patients with respiratory failure has only recently been emphasized. The effects of aminophylline on the ventricular fibrillation threshold during normal acid-base conditions and during respiratory failure were studied in anesthetized open chest dogs. The ventricular fibrillation threshold was measured by passing a gated train of 12 constant current pulses through the ventricular myocardium during the vulnerable period of the cardiac cycle. During the infusion of aminophylline, the ventricular fibrillation threshold was reduced by 30 to 40 percent of the control when pH and partial pressures of oxygen (PO2) and carbon dioxide (CO2) were kept within normal limits. When respiratory failure was produced by hypoventilation (pH 7.05 to 7.25; PCO2 70 to 100 mm Hg; PO2 20 to 40 mm Hg), infusion of aminophylline resulted in an even greater decrease in ventricular fibrillation threshold to 60 percent of the control level. These experiments suggest that although many factors may contribute to the increased incidence of ventricular arrhythmias in respiratory failure, pharmacologic agents, particularly aminophylline, may play a significant role.