Showing papers on "Hypoventilation published in 1978"

The obesity-hypoventilation syndrome.

Abstract: The triad of obesity, hypoventilation and inordinate hypersomnolence characterizes the obesity-hypoventilation syndrome. The reasons for daytime hypoventilation appear related to decreased chemical drives to breathe combined with the added physical impediment of extreme obesity. When the physiology of sleep was investigated in patients with this syndrome, intermittent nocturnal obstructive apneas were documented that produced blood gas abnormalities, arrhythmias and serious elevations of both pulmonary and systemic pressures. The obstructive apneas are due to intermittent loss of muscle tone of the tongue resulting in its prolapse against the posterior pharynx. The special importance of the obesity-hypoventilation syndrome lies in its being an example of a disorder of sleep and breathing that can appear in widely different clinical settings. Therapeutic measures include weight loss, progestational agents or permanent tracheostomy.

Hypoventilation in obstructive lung disease. The role of familial factors.

Abstract: To determine the role of familial factors in the hypoventilation of chronic obstructive lung disease we measured chemical drives to breathe in normal offspring of two groups of patients with an equal degree of obstruction. One group of five patients had repeatedly normal arterial carbon dioxide tension (PaCO2), whereas PaCO2's were elevated in the other group of six. Two adult offspring of each patient were studied. Drives were measured as the ventilatory response to isocapnic hypoxia, and the slopes of the ventilation/PCO2 relation (the hypercapnic ventilatory response). The mean response to isocapnic hypoxia was lower (P less than 0.01) in offspring of patients with high PaCO2's than in the offspring of patients with normal levels (71 +/- 7.8 [S.E.M.] vs. 113 +/- 10.3); one offspring of each patient with high PaCO2 had a response below the range found in offspring of all patients with normal PaCO2. Lower hypercapnic ventilatory responses (P less than 0.05) were also found in the offspring of patients with high PaCO2. Familial factors in the control of breathing may be an important determinant of ventilation in chronic obstructive lung disease.

Central hypoventilation syndrome: experience with bilateral phrenic nerve pacing in 3 neonates.

Abstract: Successful long-term phrenic nerve pacing has been reported in adults with acquired central hypoventilation syndrome. This report summarizes our experience with phrenic nerve pacing in 3 infants with congenital central hypoventilation syndrome. The electrodes were implanted in the lower thoracic portion of each phrenic nerve. In all patients. bilateral simultaneous pacing was required to maintain an adequate arterial PO2, tidal volume, and minute ventilation during quiet sleep. Case 1 died of problems primarily related to the severe cor pulmonale that had been present before pacemaker insertion; at autopsy, the pacemaker system was intact and there were no significant phrenic nerve abnormalities. Case 2 later developed failure of awake ventilatory control and died because of extensive phrenic nerve damage incurred by 19 days of continuous pacing. Case 3 has received quiet sleep pacemaker support since September 1977 and has been able to maintain normal quiet sleep ventilation in this manner. Phrenic nerve pacing can be successful in infants as long as continuous pacing is not required. Bilateral simultaneous pacing appears to be an appropriate alternative to home-based intermittent positive-pressure breathing for long-term management of children with central hypoventilation syndrome.

Primary alveolar hypoventilation treated by nocturnal administration of O2.

Abstract: A case of idiopathic alveolar hypoventilation is described. Although lung function was normal, the alveolar-arterial O2 tension difference was abnormally large for reasons which were unclear. Despite this, the patient's pulmonary hypertension and polycythemia were out of proportion to the relatively mild hypoxemia that he demonstrated while awake. Sleep was associated with severe hypoxemia, and administration of O2 during sleep produced CO2 retention. The patient did well on no treatment for 5 years, until respiratory infection precipitated severe hypoxemia and pulmonary hypertension. He was treated with O2, at first continuously then nocturnally (12 hours per day), with reversal of polycythemia and pulmonary hypertension. He was then treated with nocturnal O2 as an outpatient for 7 months and maintained his improvement. Nocturnal administration of O2 may be an effective treatment of some forms of primary hypoventilation.

Prolonged Doxapram Infusion in Obesity-Hypoventilation Syndrome

Abstract: Doxapram hydrochloride, a potent, centrally acting respiratory stimulant, is used to treat acute respiratory insufficiency caused by anesthetic administration, 1 drug overdose, 2 and chronic obstructive pulmonary disease. 3 We used it to treat acute respiratory failure due to the obesity-hypoventilation syndrome because the patient's condition did not improve with conventional therapy. Report of a Case A 39-year-old woman came to the hospital because she felt depressed. She also had dyspnea after walking ten to 12 steps. Her son reported that she slept approximately 12 hours per day and was difficult to arouse. She reported a weight gain of approximately 45 kg over the past year, had had pedal edema for the past four months, and there was recent onset of periorbital edema. The patient had been overweight since her teens, when she weighed 81 kg. Because of emotional stress precipitated by family problems, she began to eat excessively. Both

[O2 chemoreflex drive of ventilation in the awake rat (author's transl)].

Abstract: Resting ventilation, arterial pH and gas tensions in the arterial blood and ventilatory responses to transient O2 inhalation were studied by plethysmography, under normoxic and hypoxic (FIO2 = 0.12) conditions, in the awake rat before and after chronic bilateral denervation of the carotid bodies. 1. In the intact rat, the O2-chemoreflex drive of ventilation controlled about 50% of the normoxic minute volume, and 85% in hypoxia. 2. Chronic bilateral carotid body denervation reduced the chemoreflex drive to half, and was accompanied by a hypoventilation with arterial hypercapnia. 3. In acute hypoxia hyperventilation was reduced in carotid-body denervated animals, and was accompanied by a light respiratory insufficiency. These results suggest that the rat has a powerful arterial chemoreflex drive of breathing which is essential in determining the eupneic level of ventilation in acute hypoxia.

Severe hypercapnia associated with a non-respiratory alkalosis

Abstract: A case of hypoventilation in response to a non-respiratory alkalosis is presented. It is postulated that the degree of hypoventilation encountered was a normal response and that a fall in intracellular hydrogen ion concentration was responsible for the hypoventilation. This explains why the alkalosis associated with potassium deficiency is not associated with hypoventilation since the intracellular hydrogen ion concentration then remains constant. The renal response in this condition is responsible for maintaining the alkalosis and seems to be aimed at sodium conservation and hence plasma volume control rather than defence of acid-base balance.

Myxoedema coma. A review.

Abstract: Myxoedema coma is a rare emergency needing prompt recognition and urgent treatment before diagnostic confirmation. The pathyphysiology, clinical features, differential diagnosis, investigations and treatment are described. Triiodothyronine in small doses intravenously with continuous cardiac monitoring is suggested. Slow rewarming, care of the airway and prompt treatment of hypoventilation by assisted ventilation, the use of hydrocortisone and the avoidance of sedatives, vasopressors and overloading are also discussed, as is prevention. This emergency occurs in elderly people often with co-existent disease and thus only close attention to detail will be rewarded with improving results and falling mortality figures.

The treatment of cor pulmonale.

Abstract: COR PULMONALE is broadly defined as alteration of the structure or function of the right ventricle as a result of disease or dysfunction of the lungs.1,2The constant feature of this disorder is pulmonary hypertension in response to which the right ventricle may dilate, hypertrophy, or subsequently fail. Chronic obstructive lung disease (COLD) is the most common cause of cor pulmonale, but it also may be seen with many other lung diseases, in persons with normal lung function residing at high altitudes, or as a result of hypoventilation, as in the syndromes of primary alveolar hypoventilation or sleep apnea. PATHOPHYSIOLOGY The modern approach to the therapy of cor pulmonale is based on extensive investigation into the mechanisms that cause pulmonary hypertension and into the physiological changes that accompany it. Several excellent reviews have summarized this wealth of information.1-3It is generally agreed that the most potent stimulus to

Status asthmaticus, mechanical ventilation, and pneumothorax.

Abstract: To the Editor.— The review by Scoggin et al (238:1158, 1977) of their experience with mechanical ventilation of patients with status asthmaticus clearly demonstrates the increased incidence of certain complications (pneumothorax, pneumonia, hypoventilation, and tube malfunction). I would like to expand on the issue of pneumothoraxes in light of their discovery of two unsuspected pneumothoraxes at autopsy. As a medical housestaff officer, I was able to reverse six cardiopulmonary arrests in patients with chronic lung disease by release of a tension pneumothorax. Each of these events was thought to be a primary cardiac arrest because the initial decompensation noted was either bradycardia, ventricular tachycardia, or hypotension before a respirator alarm was triggered. Also, the physical signs of a tension pneumothorax were not detectable, as breath sounds are often severely diminished in these patients and a substantial shift in the mediastinum was not found in the circumstances of the "code." Often

Recurrent Hypersomnia Secondary to Sleep Apnea

Abstract: To the Editor.— The recent clinical note by Spira and Scheinberg ( Arch Neurol 34:513-514, 1977) in which they state that Pickwickian patients are not sleep-deprived but have a syndrome caused by hypoventilation and hypercapnia perpetuates conflicting and ambiguous terminology used for the sleep-disordered, obese, "Pickwickian" group of patients. Pickwickian syndrome should not be placed in contradistinction to other sleep-deprivation syndromes on the basis of a different etiology. The etiology of the so-called Pickwickian syndrome is, simply stated, unknown, and my experience, as well as that of others, suggests that upper airway obstruction and resulting sleep deprivation does indeed play a pathogenetic role. 1-7 The legitimate clinical entity is derived from the report by Burwell et al 8 of a case reminiscent of an adolescent boy in Dicken's Pickwick Papers with obesity and somnolence, but the syndrome includes cyanosis, pulmonary hypertension, alveolar hypoventilation, and polycythemia. Pickwickian syndrome in the less strict sense

Apneic threshold in intra-operative anesthesia.

Abstract: The depression of ventilation during general anesthesia has been recognized from the very inception of anesthetic practice1. Spontaneous breathing under general anesthesia results in hypoventilation, leading to arterial hypoxemia and hypercarbia. Therefore, the maintenance of adequate ventilation is of the utmost importance