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At least 19 recordsLinked to original sources
PubMed1994

[Management of nocturnal nasal mask continuous positive airway pressure in central hypoventilation in patients with respiratory diseases].

The effect of nasal mask CPAP administered during night in four central hypoventilation patients with various causes were investigated. On the basis of their histories, specific clinical manifestations, cranial CT and MRI, cerebral angiography and polysomnography. The patients (three males and one female) are diagnosed as primary alveolar hypoventilation and central hypoventilation, the later mainly caused by the compression of bulbar respiratory centre due to congenital deformity of right vertebral artery and deformity of foramen magnum. In order to assess the severity of nocturnal hypoventilation and blood oxygen level of the patients, polysomnography was taken before treatment, during 2L/min of oxygen via nasal tube and CPAP ventilation. Only oxygen administration did not ameliorate hypoventilation episodes and hypoxemia, lowest SaO2 is less than 50% on four patients, hypoventilation index is greater than 20 times/hour in three patients and 6.4 in a patient. Applying CPAP with the pressure fixed to 6-12 cm H2O can significantly improve hypoventilation index and hypoxemia with lowest SaO2 more than 70% (P < 0.001) and hypoventilation index less than 7 (P < 0.01). We conclude that nocturnal nasal mask CPAP is an effective treatment for central hypoventilation.

Adult↗
PubMed1985

Chronic hypoventilation and development of brain stem gliosis.

Chronic hypoventilation is important in the pathogenesis of congenital hypoventilation syndromes and sudden infant death syndrome. Cases of hypoventilation can be divided clinically into those with a defective respiratory drive and those with mechanical impairment of either the lungs or the chest wall. To determine the relationship between chronic hypoventilation and brain stem gliosis, the development of astrocytes in the brain stem of normal and abnormal cases with either type of chronic hypoventilation was studied morphometrically. The glial fibrillary acidic protein immunoperoxidase method of staining astrocytes showed a transient increase of astrocytes in some parts of the brain stem during early infancy in thirty-five normal cases. The astrocytosis was even greater in both types of chronic hypoventilation including subjects with myopathy, Ondine's curse, and sudden infant death syndrome. Gliosis in these subjects may have resulted from "asphyxia" of the brain stem, as seen in cases with myopathies involving respiratory muscles. However, the involvement of brain stem respiratory centers may suggest a failure of neural respiratory control that further compromises respiratory function.

Astrocytes↗
PubMed1982

The effects of localized hypoventilation on ventilation/perfusion (V/Q) ratios and gas exchange in the dog lung.

1. Hypoventilation of one lobe of lung was studied in open-chest anaesthetized dogs. Lobar blood flow, pulmonary-artery pressure and gas exchange were measured, the latter from breath-by-breath analysis with a mass spectrometer. 2. Hypoventilation of the lobe by reducing the respiratory pump stroke led, at each step, to a reduction in blood flow to that lobe. The flow (Q) reduction was variable, but always less than the ventilation (VE) reduction, so that the V/Q ratio to the lobe was reduced. O2 tension and pH fell and CO2 tension rose in effluent blood. Thus V/Q regulation achieved by flow reduction varied between individuals and was of low gain. 3. Anatomical or series dead space (VD series) was reduced in proportion to ventilation. When VD series was less than the apparatus dead space, some gas exchange still took place. 4. Oxygen uptake (VO2) and CO2 output (VCO2) were reduced during hypoventilation. VCO2 fell more than VO2, so that the respiratory exchange ratio (R) was reduced. 5. Whether the deterioration in gas tensions in effluent blood during hypoventilation of the lobe was due to shunt of blood past unventilated alveoli, or to V/Q mismatching, was not resolved. 6. The plateau phase of the CO2-output curves at low tidal volumes was usually regular; thus either hypoventilation was uniform, or some ventilation units were totally closed.

Animals↗
PubMed1994

Dose dependency of perceived breathlessness on hypoventilation during exercise in normal subjects.

To determine whether a dose-dependent relationship exists between the subjective sensation of breathlessness and hypoventilation during steady-state exercise, we measured breathlessness at six levels of volitionally suppressed ventilation. To achieve this, subjects targeted their breathing at 0, 5, 10, 15, 20, and 25% below their spontaneous exercise level. All 12 subjects were successful in hypoventilating in a graded manner. However, in general, the degree of hypoventilation achieved was less than that of the target level set; this discrepancy was greatest at the higher target levels. Volitional hypoventilation at target levels of > or = 10% caused significant decreases in ventilation and significant increases in end-tidal PCO2. All levels of volitional hypoventilation caused increased ratings of breathlessness, reaching statistical significance at a set target level of 15%. Significant increases in breathlessness intensity were associated with increases in end-tidal PCO2 of 2-3 Torr. We conclude that, during steady-state exercise, there appears to be a dose-dependent relationship between breathlessness and volitionally induced inappropriately low ventilation. The need to minimize such subjective sensations of breathlessness may play a role in the increased ventilation observed during exercise.

Adult↗
PubMed1994

Anxiety and congenital central hypoventilation syndrome.

OBJECTIVE: It has been hypothesized that individuals who cannot perceive elevations of CO2 will be less anxious than individuals with intact CO2 perception. To test this hypothesis, children with congenital central hypoventilation syndrome, who have a potentially lethal chronic illness associated with lack of CO2 perception and thus provide a natural experimental group, were studied. METHOD: Rates of anxiety symptoms and disorders in children with congenital central hypoventilation syndrome (N = 13) were compared with rates in an age-matched, nonreferred group of community subjects (N = 292) that included subgroups of children with asthma (N = 15) and other chronic medical illnesses (N = 66). Anxiety symptoms were assessed with information obtained from structured interviews of the parents, which provided both total symptom scores and DSM-III-R diagnoses. RESULTS: The children with congenital central hypoventilation syndrome exhibited significantly fewer anxiety symptoms than all other comparison subjects. Two of these children (15%) met criteria for anxiety disorders, a rate lower than that of the whole community group (24%) and of the chronically ill comparison subgroups (32%-47%). The largest difference in the prevalence of disorder emerged between the children with congenital central hypoventilation syndrome (15%) and those with asthma (47%). In the comparison of children with congenital central hypoventilation syndrome and children with other chronic illnesses, a priori analysis showed that the former had significantly lower rates of disorders that have been linked to panic in the literature. CONCLUSIONS: This study supports theories of anxiety that implicate CO2 perception in the pathophysiology of panic and related anxiety states.

Adolescent↗
PubMed1995

Chronic alveolar hypoventilation: a review for the clinician.

Chronic alveolar hypoventilation may present in an insidious fashion with nonspecific manifestations. The clinician should be aware of the potential for developing this condition in patients with certain thoracic and systemic diseases. Once chronic alveolar hypoventilation is confirmed with arterial blood gas analysis, a systematic evaluation can often point to the underlying etiology. As sleep in affected individuals is often associated with marked worsening of gas exchange and may also contribute to worsening daytime cardiopulmonary dysfunction, polysomnography is often indicated to determine the severity of nocturnal aberrations and to look for coexistent obstructive sleep apnea. Therapy of chronic alveolar hypoventilation often focuses on elimination of the nocturnal deterioration in gas exchange, and recent applications of noninvasive positive pressure ventilation during sleep have proven useful in the management of individuals with obesity-hypoventilation syndrome, restrictive thoracic disorders, neuromuscular diseases and central causes for hypoventilation. It is unclear whether wide-spread application of nocturnal ventilatory support to patients with chronic ventilatory failure due to chronic obstructive pulmonary disease is of long-term benefit.

Chronic Disease↗
PubMed1997

[Primary alveolar hypoventilation in adulthood].

BACKGROUND: Central alveolar hypoventilation in an adult is characterized by dysfunction of the respiratory center in the brainstem and is very rare, seen mostly secondary to neurological lesions of the brainstem. CASE DESCRIPTION: We report a 48-year-old man with primary alveolar hypoventilation associated with marked cardiac arrhythmias and hemodynamic changes. Arterial blood gas analysis revealed daytime hypoxemia and hypercapnia not explained by normal pulmonary results. All night polysomnography showed sleep fragmentation following repetitive central apneas and hypoventilation with marked hypoxemia and the lowest saturation in REM sleep. Severe nocturnal hypoxemia was accompanied by marked hypercapnia. Premature ventricular complexes occurred associated with nocturnal hypoxemia in NREM sleep while sinus arrest of up to 11.3 s were only seen associated with hypoxemia in REM sleep. Pulmonary arterial pressures were normal when the patient was awake with marked increases in pulmonary arterial pressures associated with hypoventilation and changes in arterial oxygen saturation with the patient was asleep. CONCLUSION: Nasal positive pressure ventilation was effectively able to treat central apneas and hypoventilation, nocturnal hypoxemia and cardiac arrhythmias were no longer observed. Also, daytime arterial blood gases were normal with nocturnal nasal mechanical ventilation.

Carbon Dioxide↗
PubMed1978

The obesity-hypoventilation syndrome.

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.

Apnea↗
PubMed1975

Decreased hypoxic ventilatory drive in the obesity-hypoventilation syndrome.

Most patients with extreme obesity do not exhibit alveolar hypoventilation, but an intriguing minority do. The mechanism(s) of this phenomenon remain unknown. A disorder in ventilatory control has been suggested as a major factor in the pathogenesis of the obesity-hypoventilation syndrome. Accordingly, hypoxic and hypercapnic ventilatory drives were measured in 10 patients with the typical symptoms of the syndrome: obesity, hypersomnolence, hypercapnia, hypoxemia, polycythemia and cor pulmonale. Hypoxic ventilatory drive, measured as the shape parameter A, averaged 21.9 +/- 5.35, approximately one-sixth that in normal controls, A = 126 +/- 8.6 (P less than 0.01). The ventilatory response to hypercapnia also was markedly reduced, the slope of the response averaging 0.51 +/- 0.005, or about one-third the normal value of 1.83 +/- 0.13 (P less than 0.01). This decreased responsiveness in hypoxic and hypercapnic ventilatory drive was consistent throughout the group. The depression in ventilatory drive found in the obesity-hypoventilation syndrome may be causally related to the alveolar hypoventilation manifested by these patients.

Adult↗
PubMed1988

Non-invasive conjunctival PCO2 and PO2 monitoring during hyper- and hypoventilation.

In order to evaluate potential applications of non-invasive fiberoptic conjunctival carbon dioxide (Pcj,CO2) and polarographic oxygen (Pcj,O2) sensors, we studied the effects of graded hyper- and hypoventilation on Pcj,CO2 and Pcj,O2 values in dogs. Pcj,CO2 values correlated well with Pa,CO2 (r = 0.95, n = 114); the mean Pcj,CO2--Pa,CO2 gradient was 4 +/- 3 (S.D.) Torr. Both hyper- and hypoventilation resulted in decreased Pcj,O2 values, whereas decreased Pa,O2 was observed only during hypoventilation; thus, the Pcj,O2/Pa,O2 index decreased during hyperventilation but was maintained during hypoventilation. Because both cerebral and conjunctival capillary beds vasoconstrict during hyperventilation, this methodology may assist in the non-invasive monitoring of cerebral oxygenation during cerebral resuscitation and surgery. Non-invasive Pcj,CO2 monitoring, which reflects Pa,CO2 during changes in ventilation, may be used to simplify ventilator management and weaning, as well as guide appropriate timing of arterial blood gas analysis in hemodynamically stable patients.

Animals↗
PubMed1999

Hypoventilation recruits preganglionic sympathetic fibers with inspiration-related activity in the superior cervical trunk of the rat.

Activity in preganglionic sympathetic neurons projecting in the cervical sympathetic trunk (CST) of rats was analysed with respect to changes in the pattern of the respiratory modulation during a long lasting hypoventilation. Under normal acid-base status (pH: 7.36+/-0.04, pCO2: 42.1+/-6.1 mm Hg, pO2: 135.8+/-43 mm Hg) a maximum of activity during expiration (expiration-related activity) was observed in all nerve recordings (n = 27). No other pattern of respiratory modulation was observed under this condition. Under a hypoventilation a dissociation between the duration of phrenic nerve activity and that of the inspiratory inhibition in neurons with expiration-related activity was observed as the inhibition was significantly prolonged by 49+/-24.9% and outlasted inspiration in 5/7 multifibers. When acid-base status was systematically changed (pH: 7.15+/-0.05, pCO2: 80.4+/-11.8 mm Hg, pO2: 62.8+/-17.5 mm Hg [n = 7]) by a hypoventilation lasting for several hours activity with a maximum peak during central inspiration (inspiration-related activity) emerged and disappeared when control conditions were reestablished. Neurons with expiration-related activity showed a cardiac rhythmicity (CR) of 62.5+/-14.6% (n = 27) and were inhibited to baroreceptor stimulation whereas neurons with inspiration-related activity showed no discernible CR (23.1+/-5.1%; n = 7) and were not inhibited to baroreceptor stimulation. Furthermore, expiration-related neurons were inhibited by 32.5+/-18.3% (n = 27) during noxious cutaneous stimulation while neurons with inspiration-related activity were activated by 21.5+/-12.1% (n = 7). These findings suggest that the respiratory modulation of preganglionic sympathetic activity in the CST consists of expiration-related activity in normal acid-base status. During hypoventilation neurons with inspiration-related activity are recruited. These neurons show reflex patterns distinct from expiration-related neurons and probably constitute a subgroup of sympathetic neurons which is activated under increased respiratory drive.

Adrenergic Fibers↗
PubMed1999

Ketamine antagonises alfentanil-induced hypoventilation in healthy male volunteers.

BACKGROUND: The effects of ketamine on respiration, alone, or in combination with opioids, have not been completely clarified. Both stimulant and depressant effects have been reported, as well as attenuation of opioid-induced hypoventilation at the expense of increased oxygen consumption. These conflicting results might partly be due to dose-dependent mechanisms. We have, therefore, determined the ventilatory effects of ketamine, in combination with alfentanil, using infusions to different pseudo steady-state concentrations. METHODS: On two separate days, eight healthy male volunteers were given alfentanil as a continuous computer-controlled infusion, aiming at a plasma concentration of 50 ng x mL(-1). After reaching apparent steady-state for alfentanil, racemic ketamine or placebo was administered in a protocol randomised for the two days. On the ketamine days a computer-controlled infusion, aiming for escalating ketamine plasma concentrations of 50, 100 and 200 ng x mL(-1), was added to the alfentanil infusion. On the placebo days saline was added. Using a face-mask with an occlusion valve, respiratory parameters were measured during air-breathing and after 6 repetitive 30-s CO2 challenges. RESULTS: The alfentanil infusion induced hypoventilation by decreasing respiratory rate, while tidal volume and respiratory drive were unaffected. This hypoventilation was antagonised by ketamine in a concentration-dependent manner mainly through an increase in respiratory rate. The CO2 response was not affected by alfentanil or ketamine. CONCLUSION: In the dose range of interest for postoperative, intensive-care and pain-clinic settings, ketamine antagonises the resting hypoventilation induced by alfentanil.

Adult↗
PubMed1975

Pulmonary shunting during alveolar hypoventilation in the dog.

Pulmonary shunting (Qs/Qt) was measured in 16 anesthetized and paralyzed healthy beagle puppies during a control period when the end-expired CO2 concentration was 5 per cent and during alveolar hypoventilation, when the PaCO2 increased to 100 plus or minus 13 torr (mean plus or minus SE) and the ;Ha vecame 7.04 plus or minus 0.04. A constant tidal volume was maintained throughout each study, and hypoventilation was achieved by slowing only the respiratory rate. During the control period Qs/Qt was 2.9 plus or minus 0.3 per cent; during hypoventilation Qs/Qt was 3.2 plus or minus 0.3 per cent (an insignificant difference). The puppies, therefore, responded to anesthesia and alveolar hypoventilation without development of increased pulmonary shunts.

Anesthesia, Intravenous↗
PubMed1993

Central contribution to hypoventilation during severe inspiratory resistive loads.

OBJECTIVE: Recent observations suggest that central hypoventilation with slowing of respiratory frequency contributes to hypoventilation during severe inspiratory resistive loads. We carried out a study to further characterize this bradypneic response. DESIGN: Prospective, controlled laboratory study. SETTING: Basic science laboratory of a university hospital. SUBJECTS: Anesthetized adult cats (loading experiment n = 7, nonloaded hypercapnic controls n = 11). INTERVENTIONS: Experimental inspiratory loads increased transdiaphragmatic pressure to 75% of the maximum for each animal. Respiratory responses were observed at midrun or moderate conditions of respiratory insufficiency (defined as PaCO2 > or = 60 torr [> or = 8.0 kPa]) and failure (PaCO2 > or = 80 torr [> or = 10.6 kPa]). Nonloaded hypercapnic controls were studied with similar durations of exposure to CO2 in the same CO2 range. MEASUREMENTS: Inspiratory airflow, tidal volume, respiratory frequency, airway pressure, transdiaphragmatic pressure, transdiaphragmatic pressure response to phrenic nerve electrical stimulation, blood gas analysis. Severe inspiratory loads were applied to anesthetized adult cats to determine whether bradypnea could be observed in an anesthesized model that eliminated conscious responses. Experiments were performed in hyperoxic conditions to determine whether bradypnea develops in the absence of hypoxia. An additional control group was studied under hypercapnic conditions without loading to determine whether comparable hypercapnia is a sufficient stimulus to elicit bradypnea. RESULTS: From midrun until failure, minute ventilation decreased by 16% in loaded animals. Hypoventilation was associated with a decrease in respiratory frequency from 40.1 to 29.9 breaths/min, whereas tidal volume, spontaneous transdiaphragmatic pressure, and transdiaphragmatic pressure response to phrenic nerve electrical stimulation remained unchanged. Control animals had no significant reduction in ventilation or respiratory frequency over similar levels and durations of hypercapnia. CONCLUSIONS: Centrally mediated bradypnea contributed to hypoventilation in respiratory failure associated with inspiratory loading. Bradypnea preceded evidence of muscle fatigue. This change in respiratory cycle timing occurred under anesthesia, and thus, did not depend on conscious perception of dyspnea. Bradypnea does not depend on either hypercapnia or hypoxia.

Airway Resistance↗
PubMed1983

The obesity hypoventilation syndrome and the Prader-Willi syndrome.

Fourteen children with the Prader-Willi syndrome have been managed at the Royal Alexandra Hospital for Children between the years 1964-1980--twelve male, two female. Six male children developed features of the obesity hypoventilation syndrome. The age of onset of this complication ranged from 4.0 to 12.6 years. With one exception those children with the obesity hypoventilation syndrome were more obese than those without it. At the time of onset of the syndrome, five of six patients had weights greater than or equal to 6.5 standard deviations above ideal body weight. Those children without the obesity hypoventilation syndrome had a range of standard deviations 1.0 to 4.2 above the ideal body weight. In four of six cases weight reduction and a cardiac failure regimen resulted in reversal of the obesity hypoventilation syndrome. With two of the six children there had been cardiomegaly and increased pulmonary venous vascularity on x-ray at a chronological age of three months. Two of the six children died.

Body Weight↗
PubMed1990

Cardiovascular responses to verapamil and nifedipine in hypoventilated and hyperventilated rats.

1. The influence of hypoventilation or hyperventilation on blood pressure and pulse rate responses to verapamil and nifedipine was studied in chloralose-anaesthetized rats. 2. Artificial ventilation with room air at a fixed volume of 10 ml kg-1 successfully induced combinations of hypoxaemia, hypercarbia and acidosis at a ventilator rate of 37 strokes min-1 and of hyperoxaemia, hypocarbia and alkalosis at 160 strokes min-1. 3. Hypoventilation caused significant decreases in both the blood pressure and pulse rate, whereas hyperventilation produced significant increases in these parameters. 4. In the controls, intravenous injections of graded doses of either verapamil or nifedipine caused dose-dependent decreases in mean blood pressure. The effects on pulse rate were not marked. 5. The hypotensive effects of verapamil were significantly more intense in hyperventilated rats, whereas those of nifedipine were significantly less pronounced in hypoventilated animals. The hypoventilated rats exhibited a significant dose-dependent decrease in pulse rate in response to verapamil administration. 6. It is concluded that cardiovascular responses to verapamil, nifedipine and probably other calcium antagonists are altered in the presence of blood gas abnormalities.

Animals↗
PubMed1985

Effects of hypoventilation on the cardiovascular responses of rats to adrenaline and acetylcholine.

Blood pressure and pulse rate in response to administered adrenaline and acetylcholine during hypoventilation were studied in urethane-anaesthetized rats. Hypoventilation was induced by decreasing the stroke volume of artificial ventilation from 1 ml/100 g to 0.3 ml/100 g. There was a significant rise in pulse rate accompanied by minimal changes in blood pressure during hypoventilation. The blood pressure and pulse rate in response to adrenaline were significantly reduced. The depressant effect of acetylcholine on pulse rate was intensified, but that on blood pressure was not significantly affected. These findings suggest that the compensatory cardiovascular reflexes may be impaired during hypoventilation.

Acetylcholine↗
PubMed2000

Daytime predictors of sleep hypoventilation in Duchenne muscular dystrophy.

Sleep hypoventilation is an inevitable consequence of Duchenne muscular dystrophy (DMD), usually preceding daytime respiratory failure. Appropriate scheduling of polysomnography and the introduction of noninvasive ventilation (NIV) during sleep are not defined. Our aim was to determine the parameters of daytime lung function associated with sleep hypoventilation in patients with DMD. As our method we chose a prospective comparison of wakeful respiratory function (spirometry, lung volumes, maximal mouth pressures, arterial blood gases) with outcomes of polysomnography. All measurements were made with subjects breathing air. Nineteen subjects were studied. The FEV(1) was correlated with Pa(CO(2)) (r = -0.70, p < 0.001) and base excess (r = -0.68, p < 0.01). All of these parameters were significantly related to sleep oxygenation (proportion of total sleep time spent at an Sa(O(2)) </= 90% [TST < 90%]). An FEV(1) < 40% was a sensitive (91%) but not specific (50%) indicator of sleep hypoventilation (TST < 90% of >/= 2%); a Pa(CO(2)) of >/= 45 mm Hg was an equally sensitive (91%) but more specific (75%) indicator while a base excess of >/= 4 mmol/L was highly specific (100%) but less sensitive (55%). After introduction of NIV during sleep (n = 8), there was a significant reduction in wakeful Pa(CO(2)) (54 +/- 7.4 to 49.1 +/- 4 mm Hg, p < 0.02) over 0. 9 +/- 0.4 yr despite a further decline in FEV(1) (0.84 +/- 0.46 to 0. 64 +/- 0.39 L, p < 0.05). We conclude that in patients with DMD, (1) arterial blood gases should be performed once the FEV(1) falls below 40% of the predicted value; (2) polysomnography should be considered when the Pa(CO(2)) is >/= 45 mm Hg, particularly if the base excess is >/= 4 mmol/L; (3) the decrease in wakeful Pa(CO(2)) after NIV administered during sleep implicates sleep hypoventilation in the pathogenesis of respiratory failure; and (4) impaired ventilatory drive is a possible mechanism for respiratory failure, as the NIV-associated decrease in wakeful Pa(CO(2)) occurs despite a further decline in ventilatory capacity, suggesting continuing deterioration in respiratory muscle function.

Adolescent↗