Showing papers on "Hypoventilation published in 1984"

Sleep in the Prader-Willi Syndrome: Clinical and Polygraphic Findings

Abstract: • Nine patients with the Prader-Willi syndrome, ranging in age from 3 to 21 years, were examined clinically as well as studied in the sleep laboratory. They had striking disturbances of sleep-wakefulness patterns. All patients except one had the symptom of excessive daytime sleepiness. The most striking finding was the presence in five patients of rapid-eye-movement (REM) sleep occurring at sleep onset (SOREM). None of the patients had the condition of sleep apnea. One patient, however, demonstrated severe hypoventilation during REM sleep; the lowest value recorded for O2saturation was 40%, with a consistent value below 50% for as long as ten to 15 minutes. Previous findings have indicated that the Prader-Willi syndrome is of hypothalamic origin. We hypothesize that both the SOREM and O2desaturation findings in our patients with the Prader-Willi syndrome are also a result of hypothalamic changes.

Accessory muscle activity during sleep in chronic obstructive pulmonary disease

Abstract: Hypoventilation contributes to oxyhemoglobin desaturation during rapid-eye-movement (REM) sleep in patients with severe chronic obstructive pulmonary disease (COPD). Due to hyperinflated lungs these patients have mechanically impaired diaphragms and increased activity of other inspiratory muscles while awake. We speculated that rib cage (RC) inspiratory muscles might lose activity during REM, thereby contributing to hypoventilation. We therefore recorded scalene (SCA) and sternocleidomastoid (SCM) electromyorgrams in six subjects with severe COPD. SCA activity decreased 76% (P less than 0.001), from non-REM (NREM) to tonic REM and decreased an additional 17% during phasic REM. SCM activity was much more variable during NREM but when present also decreased during REM. SCA activity correlated strongly with RC excursion. SCA and SCM activity, RC excursion, estimates of minute ventilation, and oxyhemoglobin saturation all decreased in parallel. Expiratory activity of the SCA and SCM, present during wakefulness and NREM, disappeared during REM. We conclude that loss of inspiratory activity of rib cage muscles during REM causes chest wall distortion and hypoventilation in patients with severe COPD. Loss of expiratory activity of these muscles may contribute to a decrease in end-expiratory volume and thereby to a deterioration of pulmonary gas exchange.

Mechanisms producing hypoxemia during hemodialysis.

Abstract: Arterial hypoxemia occurs frequently during hemodialysis. Proposed mechanisms for this phenomenon have included hypoventilation and embolism of granulocyte aggregates. We studied 18 patients with endstage renal failure who required chronic hemodialysis, and measured arterial blood gases, pulmonary gas exchange, and dialyzer gas exchange. During use of acetate as a dialysate buffer, PaO2 decreased to 80 +/- 6.8 torr, whereas during use of the bicarbonate buffer oxygen tension remained at 92 +/- 4.9 torr or greater. Hypoventilation and microembolism were not sufficient to explain the degree of hypoxemia during acetate dialysis. Hypoxemia occurred only after the 1st exposure to acetate; neither an instantaneous change to bicarbonate nor stopping dialysis restored oxygen tension to normal. We conclude that a pharmacologic action of acetate adversely affects lung function, aggravating the decreased alveolar oxygen tension (PAO2) due to hypoventilation. Hypoxemia was not present when bicarbonate was used. Acetate buffer should not be used for dialysis in patients with unstable cardiovascular or respiratory systems.

Reversible hypercapnic respiratory insufficiency in scleroderma caused by respiratory muscle weakness.

Abstract: A patient with scleroderma presented with hypercapnic respiratory failure. Evaluation of pulmonary mechanics revealed severe restriction caused in part by respiratory muscle weakness. Treatment with prednisone corrected hypoventilation, improved symptoms, increased lung volumes, returned respiratory muscle strength to normal range, but did not change the degree of lung stiffness. This case demonstrates that restrictive patterns in scleroderma can be due to either lung or chest wall disease and that the latter may be reversible. If respiratory muscle weakness is present with restrictive ventilatory patterns in patients with scleroderma, a therapeutic trial of corticosteroid is warranted.

Transcutaneous CO2 monitoring and disordered breathing during sleep.

Abstract: A new device for non-invasive monitoring of PCO2, the Hewlett Packard cutaneous capnometer, was studied. Seven patients with disordered breathing, three with sleep apnoea syndrome, and four with chronic respiratory insufficiency, underwent polygraphic sleep recording including non-invasive measurement of oxygen saturation and transcutaneous CO2 pressure (PtcCO2). Two of the apnoea patients showed a modest increase in PtcCO2 with sleep. The patients with respiratory insufficiency showed larger increase in PtcCO2 and more profound hypoxemia during sleep. When the patients with respiratory insufficiency received oxygen (0.3-0.5 l/min) via nasal prongs, the sleep induced hypoxemia almost vanished but their PtcoCO2 increased. Nocturnal hypoventilation probably increased the effectiveness of the low oxygen supply, thus counteracting hypoxemia during periods of hypoventilation. The capnometer was easy to apply and the patients felt no discomfort. It promises to be a useful method for detection of hypercapnia indicating hypoventilation in patients with disordered breathing.

Life threatening hypoventilation in kyphoscoliosis: successful treatment with a molded body brace-ventilator.

Abstract: We report sustained successful treatment of end-stage hypoventilation in a 37-yr-old patient with kyphoscoliosis caused by childhood poliomyelitis. The patient presented with progressive ventilatory failure, pure restrictive lung function, and no concurrent illness. He first responded to respiratory stimulation with medroxyprogesterone acetate and aminophylline. Because of skeletal deformity and the need for a chronic brace he was then fitted with a customized polyethylene foam body brace with an anterior free space and connecting hole for a Monaghan ventilator. No longer taking any medication, and with only nocturnal assisted ventilation, he now has normal daytime arterial blood gas values 20 months later. This approach may be useful in other patients with severe kyphoscoliosis.

A polygraphic study of one case of primary alveolar hypoventilation (Ondine's curse).

Abstract: We report here on a case of primary alveolar hypoventilation in a 9 yr old child. From the age of 8 years, the patient has suffered from episodes of bronchopneumonia associated with severe respiratory insufficiency and lethargy. After recovery, cyanosis developed during the night and, later on, during the day. On two occasions, serious respiratory depression followed ketamine sedation for cardiac catheterization and total anaesthesia for cerebral angiography. Pulmonary function tests showed normal volumes and normal mechanics of breathing; blood gas analysis revealed a slight hypercapnic acidosis and hypoxia. The ventilatory response to CO2 was virtually absent, whereas voluntary hyperventilation normalized blood gas values. A polygraphic recording during sleep showed a marked worsening of hypoventilation, which occurred soon after falling asleep and continued throughout all sleep stages; sporadic central apnoeas, at times prolonged, were recorded only during light sleep. The patient, now 14 yr old, is maintained in satisfactory condition with low flow nocturnal oxygen administration combined with the use of a body respirator during sleep twice a week.

Renal Tubular Acidosis

Abstract: The body maintains normal acid-base equilibrium by respiratory and renal control of buffers, especially bicarbonate. The respiratory system influences acid-base equilibrium by hyperventilation, with primary or secondary respiratory alkalosis (with low PCO2), or by hypoventilation, leading to respiratory acidosis (with very high PCO2). The kidney is the body’s other major site for acid-base control. Daily the kidney normally accounts for secretion of 4500 mEq of acid/1.73 m2 in exchange for the reabsorption of all filtered bicarbonate and, in addition, the secretion of 1–2 mEq/kg acid in the form of titrable acid and ammonium. A brief review of how the normal kidney performs this acidification will be necessary to consider adequately the appropriate therapeutic responses to the renal tubular acidoses.