Showing papers on "Hypoventilation published in 1980"

A new method for noninvasive bedside determination of pulmonary blood flow.

Abstract: A method is presented for determining the pulmonary blood flow from measurements of the time-averaged end-tidal pCO2 and the CO2 output.

Congenital Central Hypoventilation and Sleep State

Abstract: Congenital central hypoventilation (Ondine9s curse) is described in an infant with persistant symptoms throughout the first nine months of life. Respiratory control was most severely affected in quiet sleep, although abnormalities were present in rapid eye movement (REM) sleep and while awake. Failure of metabolic control in quiet sleep led to profound hypoventilation. Behavioral or "behavioral-like" inputs in the awake state and REM sleep increased ventilation, but not to expected normal levels. The ventilatory response to inhaled 4% CO2 was markedly depressed in all states.

Incidence of metabolic alkalemia in hospitalized patients

Abstract: Analysis of 13,430 arterial blood samples demonstrated that metabolic alkalemia was the most common acid-base disturbance encountered in the hospital setting, being present in 51% of patients with abnormal acid-base status. Respiratory alkalemia was encountered in 29%, respiratory acidemia in 27%, and metabolic acidemia in only 12%. Evaluation of those blood gases with metabolic alkalemia, using 95% confidence-limit bands for acid-base disturbances, showed that the metabolic alkalemia was pure in 70% of the cases, mixed with respiratory acidemia in 18%, and combined with respiratory alkalemia in 12%. The adverse effects of alkalemia may be subtle but often significant. Alveolar hypoventilation in response to metabolic alkalemia, without evidence of primary respiratory disease, was more frequent than is generally suspected. This hypoventilation often directly results in hypoxemia, as well as atelectasis with worsened ventilation/perfusion match-up. Alkalemia shifts the oxyhemoglobin dissociation curve to the left, increasing hemoglobin's affinity for oxygen, thus, limiting oxygen release at the tissue level. The presence of metabolic alkalemia makes it more difficult to wean patients from assisted ventilation. A clearer understanding of the frequency and significance of metabolic alkalemia should lead to more appropriate therapy to prevent or correct this acid-base disturbance and should result in a decreased morbidity and mortality in critically ill patients.

The effect of nasal obstruction in infancy and early childhood upon ventilation

Abstract: To evaluate the effect of nasal obstruction in infants and young children upon ventilation during sleep, change of ventilation was followed by polygraphic recordings of esophageal pressure, tidal volume and percutaneous oxygen tension when the nostrils were mechanically obstructed in 10 subjects; 3 types of ventilatory changes were noted. In 4 subjects periodic breathing appeared in which hypoventilation was alternated with occasional hyperventilation. Esophageal pressure, tidal volume and PO2 showed concomittant fluctuation. PO2 lowered during hypoventilatory phase was compensated by periodic hyperventilation. In 5 subjects upper airway obstruction was compensated for by increased respiratory endeavor and tidal volume and PO2 remained normal in spite of markedly increased esophageal pressure. In 1 subject tidal volume and PO2 remained decreased with marked increase of esophageal pressure. Largest airway obstruction was noted between the upper and the lower lips.

Management of hypoventilation in motor neuron disease presenting with respiratory insufficiency

Abstract: A 57-year-old man presented with a three-month history of somnolence, hypoventilation, cor pulmonale, and episodes of apnea during sleep. Neurological studies revealed motor neuron disease, mainly confined to the muscles of respiration, that was causing respiratory insufficiency in the supine position. Nighttime treatment of respiratory insufficiency has permitted independent activity during wakefulness.

Characteristics and surgical management of respiratory complications accompanying pathologic lesions of the brain stem.

Abstract: Three life-threatening respiratory complications are regularly encountered in patients who survive the initial insult from a diffuse brain stem lesion--central alveolar hypoventilation, upper airway obstruction, and aspiration pneumonitis. From treating 13 patients who did survive, a surgical plan for managing the respiratory sequelae of such injuries has evolved and consists of: 1)Diaphragm pacing to correct hypoventilation; 2) tracheostomy for bypass of the upper airway obstruction; 3) gastrostomy for bypass of the impaired structures of swallowing; 4) surgical closure of the larynx to prevent aspiration. All 13 patients manifested central apnea, which was controlled in five by bilateral phrenic nerve stimulation and in eight by unilateral stimulation. All patients required tracheostomy to provide an airway for artificial ventilation and for secretion removal. In ten patients aspiration necessitated gastrostomy. The spontaneous recovery of the ability to swallow allowed closure of the gastrostoma in three but in others aspiration remained a serious complication. One patient died of massive aspiration after discharge from the hospital. Three patients had surgical closure of the larynx to prevent aspiration. Seven patients are alive; six of them are leading productive lives, though several have severe disability due to paresis or ataxia. Six died after discharge from the hospital. Three deaths were not related to the basic problem but the three others may have been.

Hypokalemic hypoventilation complicating severe diabetic ketoacidosis.

Abstract: Hypokalemia has been previously reported as a cause for respiratory impairment complicating therapy for diabetic ketoacidosis. A case is presented with a short interval of hypoventilation documented by hypercapnia. A reversal from hypercapnia to hypocapnia occurred when the serum potassium level became normal after potassium replacement. Causes of muscular weakness other than hypokalemia were considered unlikely on the basis of clinical and laboratory data. The present report records the occurrence of hypoventilation associated with hypokalemia in diabetic ketoacidosis and serves to underscore the need for adequate potassium replacement during the treatment of this disorder.

Pathophysiologic mechanisms causing sleep apnea and hypoventilation in infants.

Abstract: Complete absence of chemoreception in the medulla is characterized by sustained hypoventilation. Except for the first months of life, this deficit does not, of itself, cause apnea. Both in infants who lack central chemical drive, as well as those who are only partly deficient, it is necessary to invoke at least one further pathophysiologic event. Various alterations in gas exchange, especially during sleep, which promote hypoxemia can contribute to a positive feedback effect on ventilation. If gas exchange is further impeded by upper-airway obstruction, only a massive arousal response separates the infant from death.

Analysis of ventilatory depression by enflurane during clinical anesthesia.

Abstract: Tracheal pressures during airway occlusion (an index of ventilatory drive), inspiratory time, alveolar ventilation, and PaCO2 were measured in spontaneously breathing, healthy patients during enflurane:N2O anesthesia at various inspired concentrations of enflurane. The purpose was to describe more clearly the mechanism of intraoperative hypoventilation. Occlusion pressures, inspiratory time, and alveolar ventilation were less, and PaCO2 was higher, at deeper levels of anesthesia. Hypoventilation is due to reduced mechanical transform of neuromuscular drive and to shorter inspiratory time and, therefore, reduced mean inspiratory flow rate without change in breathing frequency. Effective elastance (an index of lung stiffness) was slightly greater at deeper levels of anesthesia.

Respiratory adaptations in acid-base disturbances: role of cerebral fluids.

Abstract: : The respiratory and metabolic components of acid-base homeostasis are defined. A quantitative empirical description of the (incomplete) mutual compensations in steady acid-base disturbances primarily occurring in either of the two components is presented, based upon data compiled from the literature. Respiratory adaptations in steady acid-base disturbances of metabolic origin (hyperventilation with hypocapnia in primary metabolic acidosis, and hypoventilation with hypercapnia in metabolic alkalosis) are analyzed as a function of the acidity of the cerebral fluids (cerebrospinal and cerebral interstitial fluid). (Author)

Voluntary heart-rate changes mediated by muscle tension and respiration.

Abstract: 20 undergraduates completed heart-rate mediation treatments (isometric exercise, relaxation, hyperventilation, and hypoventilation) with and without feedback. Heart rate increased during tension, decreased with relaxation, and changed even more with feedback. During hyperventilation the heart rates were lower than during hypoventilation, and this difference was even greater during trials with feedback. This paradoxical finding was attributed to the shallowness of the breathing. Additional data from an experiment on voluntary heart-rate control (n = 31) without feedback and one with biofeedback of heart rate (n = 18) showed that subjects were following heart-rate increase and decrease instructions with altered respiration rates. These observations are interpreted as indicating that biofeedback changes in heart rate are mediated by skeletal muscle tension, respiration, and other mediating mechanisms.