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At least 19 recordsLinked to original sources
PubMed2002

[Alveolar hypoventilation in the obese: the obesity-hypoventilation syndrome].

The obesity-hypoventilation syndrome (or alveolar hypoventilation in the obese) is a new name for an old syndrome, Pickwickian syndrome. It is defined as chronic alveolar hypoventilation (PaO(2)<70 mmHg, PaCO(2) > 45 mmHg) in obese patient with a body mass index > 30 kg/m(2) who have no other respiratory disease explaining the gas anomalies. The large majority of obese subjects are not hypercapnic, even in case of severe obesity. There are three principal causes explaining alveolar hypoventilation in obese subjects: high cost of the work of respiration, dysfunction of the respiratory centers, repeated episodes of nocturnal obstructive apnea. The obesity-hypoventilation syndrome is generally found in males aged over 50 years. Exercise-induced breathlessness is a constant finding. Diagnosis is often made after an episode of severe respiratory failure. Associated diseases favored by obesity are frequent: diabetes, high blood pressure, heart disease. By definition, there is a hypoxemia-hypercapnia syndrome persisting after an acute episode. Spirography usually demonstrates moderate volume restriction. Pulmonary hypertension is frequent but not constant. Obesity-hypoventilation syndrome must be distinguished from obstructive sleep apnea, although the two conditions are often associated. Obstructive sleep apnea may be absent in certain patients with obesity-hypoventilation syndrome (we have had several cases) and inversely, obesity is not observed in certain patients with obstructive apnea. It should be recalled that the term Pickwickian syndrome designates obesity-hypoventilation syndrome (with or without obstructive apnea) and not obstructive sleep apnea syndrome.

Hemodynamics↗
PubMed2004

Obesity-associated hypoventilation in hospitalized patients: prevalence, effects, and outcome.

BACKGROUND: Severe obesity is associated with hypoventilation, a disorder that may adversely affect morbidity and mortality. We sought to determine the prevalence and effects of obesity-associated hypoventilation in hospitalized patients. METHODS: Consecutive admissions to internal medicine services were screened over a 6-month period. In all eligible subjects with severe obesity (body mass index > or =35 kg/m2), we administered a sleep questionnaire, and performed neuropsychological, arterial blood gas, and pulmonary function testing. Hospital course and mortality at 18 months was also determined. RESULTS: Of 4,332 admissions, 6% (n = 277) of patients were severely obese, of whom 150 were enrolled, 75 refused to participate, and 52 met the exclusion criteria. Hypoventilation (mean [+/- SD] arterial partial pressure of carbon dioxide [PaCO2], 52 +/- 7 mm Hg) was present in 31% (n = 47) of subjects who did not have other reasons for hypercapnia. Decreased objective attention/concentration and increased subjective sleepiness were present in patients with obesity-associated hypoventilation compared with in severely obese hospitalized patients without hypoventilation (simple obesity group; mean PaCO2, 37 +/- 6 mm Hg). There were higher rates of intensive care (P = 0.08), long-term care at discharge (P = 0.01), and mechanical ventilation (P = 0.01) among subjects with obesity-associated hypoventilation. Therapy for hypoventilation at discharge was initiated in only 6 (13%) of the patients with obesity-associated hypoventilation. At 18 months following hospital discharge, mortality was 23% in the obesity-associated hypoventilation group as compared with 9% in the simple obesity group (hazard ratio = 4.0; 95% confidence interval: 1.5 to 10.4]. CONCLUSION: Hypoventilation frequently complicates severe obesity among hospitalized adults and is associated with excess morbidity and mortality.

Adult↗
PubMed2003

Hypoventilation improves oxygenation after bidirectional superior cavopulmonary connection.

OBJECTIVE: Bidirectional superior cavopulmonary connection may be complicated by systemic hypoxemia. Previous work has shown that hyperventilation worsens systemic oxygenation in patients after bidirectional superior cavopulmonary connection. The likely mechanism is that hyperventilation-induced hypocarbia decreases cerebral, superior vena caval, and pulmonary blood flow. The aim of the current study was to determine whether the converse approach, hypoventilation, improves oxygenation after bidirectional superior cavopulmonary connection. METHODS: This is a prospective, patient-controlled study of 15 patients (median age 8.0 months, range 4.7-15.5) who underwent bidirectional superior cavopulmonary connection. Patients were studied in the intensive care unit, within 8 hours of surgery, while sedated, paralyzed, and mechanically ventilated. To avoid acidosis during hypoventilation, sodium bicarbonate was administered before hypoventilation. Cerebral blood flow velocity was measured by transcranial Doppler sonography of the middle cerebral artery. RESULTS: Hypoventilation following administration of sodium bicarbonate (pH-buffered hypoventilation) produced hypercarbia (mean Pco(2) = 58 mm Hg versus 42 mm Hg at baseline). During hypoventilation, there were significant increases in both mean arterial Po(2) (from 50 mm Hg at baseline to 61 mm Hg; P <.05) and mean systemic oxygen saturation (from 86% at baseline to 90%; P <.05). These increases occurred despite accompanying, small increases in pulmonary artery pressure and transpulmonary gradient. Hypoventilation also produced an increase in mean cerebral blood flow velocity (from 37 cm/s at baseline to 55 cm/s; P <.05) and a decrease in the arteriovenous oxygen saturation difference across the upper body (from 33% at baseline to 23%; P <.05), consistent with increased cerebral blood flow. CONCLUSIONS: This study demonstrates that hypoventilation improves systemic oxygenation in patients after bidirectional superior cavopulmonary connection. The likely mechanism for this effect is that hypoventilation-induced hypercarbia decreases cerebral vascular resistance, thus increasing cerebral, superior vena caval, and pulmonary blood flow. Hypoventilation may be a useful clinical strategy in patients who are hypoxemic in the early postoperative period after bidirectional superior cavopulmonary connection.

Acid-Base Equilibrium↗
PubMed2006

Characterization of dermatoglyphics in PHOX2B-confirmed congenital central hypoventilation syndrome.

OBJECTIVE: Individuals with congenital central hypoventilation syndrome have characteristic variants in the PHOX2B gene (primarily polyalanine expansion mutations). The PHOX2B gene acts as a transcriptional activator in the promotion of pan-neuronal differentiation in the autonomic nervous system during early embryologic development, with a primary role in the sympathetic noradrenergic phenotype in vertebrates. Because sympathetic innervation has been hypothesized to affect the development of dermatoglyphic pattern types, we hypothesized that individuals with PHOX2B-confirmed congenital central hypoventilation syndrome would have characteristic dermatoglyphic patterning and that the dermatoglyphic phenotype would be related to the disease-defining PHOX2B genotype. METHODS: Dermatoglyphic pattern type frequency, left/right symmetry, and genotype/phenotype correlation were assessed for 33 individuals with PHOX2B-confirmed congenital central hypoventilation syndrome and compared with published control data. RESULTS: Dermatoglyphic pattern type frequencies were altered in congenital central hypoventilation syndrome cases versus controls. In particular, there was an increase of arches in females and ulnar loops in males, with the largest differences for the left hand and for individuals with both congenital central hypoventilation syndrome and Hirschsprung disease. Dissimilarity scores between the congenital central hypoventilation syndrome and congenital central hypoventilation syndrome + Hirschsprung disease cases were not significantly different, nor were dissimilarity scores between all of the female and all of the male cases. No significant association was found between the number of polyalanine repeats in the PHOX2B genotypic category and dermatoglyphic pattern frequencies in the congenital central hypoventilation syndrome study groups. CONCLUSIONS: These results represent the first report describing specific dermatoglyphic patterning in congenital central hypoventilation syndrome and suggest a relationship between PHOX2B and the expression of dermatoglyphic pattern types. An expanded congenital central hypoventilation syndrome data set to include the full spectrum of PHOX2B mutations is necessary to further delineate the role of PHOX2B in dermatoglyphic patterning.

Adolescent↗
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↗
PubMed2000

Nocturnal mechanical ventilation for chronic hypoventilation in patients with neuromuscular and chest wall disorders.

BACKGROUND: Chronic alveolar hypoventilation is a common complication of many neuromuscular and chest wall disorders. Long term nocturnal mechanical ventilation is used to treat an increasing number of patients. OBJECTIVES: To examine the efficacy of nocturnal mechanical ventilation in relieving hypoventilation related symptoms in patients with neuromuscular or chest wall disorders. SEARCH STRATEGY: Search of the Cochrane Neuromuscular Disease Group register for randomized trials and enquiry from authors of trials and other experts in the field. SELECTION CRITERIA: Types of studies: quasi-randomized or randomized controlled trials TYPES OF PARTICIPANTS: patients with neuromuscular or chest wall disorder-related stable chronic hypoventilation of all ages and all degrees of severity. Types of interventions: any type and any mode of nocturnal mechanical ventilation. Types of outcome measures: Primary: short term and long term reversal of hypoventilation related clinical symptoms Secondary: unplanned hospital admission rate, one year mortality, short term and long term reversal of day time hypercapnia, improvement of lung function and improvement of sleep breathing disorders. DATA COLLECTION AND ANALYSIS: We identified four randomized trials. One author extracted the data and another checked them. Individual data were available from the authors of the largest study. MAIN RESULTS: The four eligible trials included a total of 51 patients. The risk difference (proportion of patients) of no improvement of hypoventilation related clinical symptoms in the short term following nocturnal mechanical ventilation was significant and favoured treatment, -0.417 (95% CI -0.639 to -0.194). However, there was significant heterogeneity across the studies (p<0.001). Similarly, the risk difference of no reversal of day time hypercapnia in the short term following nocturnal ventilation was significant and favoured treatment, -0.635 (95% CI -0.874 to -0.396). The weighted mean difference of nocturnal mean oxygen saturation percent was 5.5 (95% CI 1.5 to 9.4) more improvement in patients treated with nocturnal mechanical ventilation. For the primary and most of the secondary outcome measures there was no significant difference between nocturnal mechanical ventilation and no ventilation in the long term, except for one-year mortality. Indeed, the risk difference of death one year following implementation of nocturnal mechanical ventilation was significant and favoured treatment, -0.259 (95% CI -0.478 to -0. 041). However, there was significant heterogeneity across the studies (p<0.001). Most of the secondary outcomes were not assessed in the eligible trials. No data could be summarised for the comparisons between invasive and non-invasive mechanical ventilation, between intermittent positive pressure and negative pressure ventilation, and between volume-cycled and pressure-cycled ventilation. REVIEWER'S CONCLUSIONS: Current evidence about the therapeutic benefit of mechanical ventilation is weak, but consistent, suggesting alleviation of the symptoms of chronic hypoventilation in the short term, and in two small studies survival was prolonged. Mechanical ventilation should be offered as a therapeutic option to patients with chronic hypoventilation due to neuromuscular diseases. Further larger randomized trials are needed to confirm long term beneficial effects of nocturnal mechanical ventilation on quality of life, morbidity and mortality, to assess its cost-benefit ratio, and to compare the different types and modes of ventilation.

Chronic Disease↗
PubMed2003

Preconditioning by hypoventilation increases ventricular arrhythmia threshold in Wistar rats.

Hypoventilation, as one of ventilatory disorders, decreases the electrical stability of the heart similarly as ischemia. If preconditioning by short cycles of ischemia has a cardioprotective effect against harmful influences of a prolonged ischemic period, then preconditioning by hypoventilation (HPC) can also have a similar effect. Anesthetized rats (ketamine 100 mg/kg + xylasine 15 mg/kg i.m., open chest experiments) were subjected to 20 min of hypoventilation followed by 20 min of reoxygenation (control group). The preconditioning (PC) was induced by one (1PC), two (2PC) or three (3PC) cycles of 5-min hypoventilation followed by 5-min reoxygenation. The electrical stability of the heart was measured by a ventricular arrhythmia threshold (VAT) tested by electrical stimulation of the right ventricle. Twenty-minute hypoventilation significantly decreased the VAT in the control and 1PC groups (p<0.05) and non-significantly in 2PC vs. the initial values. Reoxygenation reversed the VAT values to the initial level only in the control group. In 3PC, the VAT was increased from 2.32+/-0.69 mA to 4.25+/-1.31 mA. during hypoventilation (p<0.001) and to 4.37+/-1.99 mA during reoxygenation (p<0.001). It is concluded that cardioprotection against the hypoventilation/ reoxygenation-induced decrease of VAT proved to be effective only after three cycles of HPC.

Acid-Base Equilibrium↗
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↗
PubMed2004

Supplemental oxygen impairs detection of hypoventilation by pulse oximetry.

STUDY OBJECTIVE: This two-part study was designed to determine the effect of supplemental oxygen on the detection of hypoventilation, evidenced by a decline in oxygen saturation (Spo(2)) with pulse oximetry. DESIGN: Phase 1 was a prospective, patient-controlled, clinical trial. Phase 2 was a prospective, randomized, clinical trial. SETTING: Phase 1 took place in the operating room. Phase 2 took place in the postanesthesia care unit (PACU). PATIENTS: In phase 1, 45 patients underwent abdominal, gynecologic, urologic, and lower-extremity vascular operations. In phase 2, 288 patients were recovering from anesthesia. INTERVENTIONS: In phase 1, modeling of deliberate hypoventilation entailed decreasing by 50% the minute ventilation of patients receiving general anesthesia. Patients breathing a fraction of inspired oxygen (Fio(2)) of 0.21 (n = 25) underwent hypoventilation for up to 5 min. Patients with an Fio(2) of 0.25 (n = 10) or 0.30 (n = 10) underwent hypoventilation for 10 min. In phase 2, spontaneously breathing patients were randomized to breathe room air (n = 155) or to receive supplemental oxygen (n = 133) on arrival in the PACU. MEASUREMENTS AND RESULTS: In phase 1, end-tidal carbon dioxide and Spo(2) were measured during deliberate hypoventilation. A decrease in Spo(2) occurred only in patients who breathed room air. No decline occurred in patients with Fio(2) levels of 0.25 and 0.30. In phase 2, Spo(2) was recorded every min for up to 40 min in the PACU. Arterial desaturation (Spo(2) < 90%) was fourfold higher in patients who breathed room air than in patients who breathed supplemental oxygen (9.0% vs 2.3%, p = 0.02). CONCLUSION: Hypoventilation can be detected reliably by pulse oximetry only when patients breathe room air. In patients with spontaneous ventilation, supplemental oxygen often masked the ability to detect abnormalities in respiratory function in the PACU. Without the need for capnography and arterial blood gas analysis, pulse oximetry is a useful tool to assess ventilatory abnormalities, but only in the absence of supplemental inspired oxygen.

Aged↗
PubMed2000

Nocturnal hypoventilation in chronic respiratory failure (CRF) due to neuromuscular disease.

Decrease of respiratory muscle capacities in neuromuscular disease can lead to chronic respiratory failure with permanent alveolar hypoventilation. Respiratory centers elaborate a strategy of breathing dedicated to prevent overt respiratory muscles fatigue. This strategy may worsen chronic hypercapnia. During sleep, ventilation decreases because a lessening in respiratory centers function. During NREM sleep hypoventilation is only an exacerbation of what is seen during wakefulness. During REM sleep, atonia worsens much more hypoventilation particularly when diaphragmatic function is impaired. The effects of atonia are amplified by a very low reactivity of respiratory centers. Nocturnal mechanical ventilation improves nocturnal hypoventilation and daytime arterial blood gases (ABG). Mechanism of improvement in ABG and how nocturnal hypoventilation and diurnal hypoventilation interact, are still a matter of debate.

Arousal↗
PubMed2005

[Alveolar hypoventilation during sleep and domiciliary assisted ventilation].

INTRODUCTION: An alveolar hypoventilation physiologically occurs during sleep and more specifically during REM sleep. STATE OF THE ART: During obstructive chronic respiratory failures, increases in PaCO2 that are associated with REM sleep can participate to the severity of daytime hypercapnia and in a subgroup of patients lead to an indication of nocturnal non-invasive ventilation (NIV) in association with the long-term oxygen therapy. A REM sleep hypoventilation generally appears during the early course of restrictive chronic respiratory failures. This REM sleep hypoventilation represents one of the most frequent reasons for initiating NIV in restrictive respiratory insufficiencies. Obesity-hypoventilation syndrome (OHS) refers to a hypercapnic chronic respiratory failure in which REM sleep hypoventilation is one of the main determinants. In France, in 2004, OHS is the primary chronic respiratory failure leading to at home NIV. NIV on OHS aims to maintain upper airway patency as sleep apnoea is frequently associated and to allow sufficient alveolar ventilation during REM sleep. PERSPECTIVES: Thus, sleep alveolar hypoventilation should be systematically assessed in obese patients and during the time curse evolution of all the chronic respiratory failures. This can be done relatively easily by using nocturnal oximetry concurrently with a transcutaneous PCO2 measurement. CONCLUSION: The understanding of exact mechanisms underlying abnormal respiratory events occurring during sleep allows optimising adjustments in NIV parameters.

Chronic Disease↗
PubMed2002

[Central alveolar hypoventilation syndrome and cerebral venous thrombosis: fortuitous association?].

UNLABELLED: Central hypoventilation syndrome is defined as the failure of automatic control of breathing. Secondary central hypoventilation syndrome should distinguish from congenital central hypoventilation syndrome by brainstem abnormalities, place of respiratory control. CASE REPORTS: We report two clinical cases characterized by late onset central hypoventilation syndrome (three years--six months, and five years old): in the first case the diagnosis was made after general anesthesia and the second one presented with acute nocturnal comatose state. Neuroradiologic investigations showed bilateral cerebral sinus veinous thrombosis without any brainstem lesions. Moreover these children had severe behavior disorders: psychomotor instability, alterations of social relations, language dysfunction, and neurocognitive deficit. This symptomatology seems independent from central hypoventilation syndrome and cerebral venous thrombosis. CONCLUSION: Late onset central hypoventilation syndrome may be associated with cerebral venous thrombosis. Ischemia of central chemoreceptors or integration of their informations could be one of mechanism.

Child, Preschool↗
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↗
PubMed2005

Effects of xenon anaesthesia on the circulatory response to hypoventilation.

BACKGROUND: Circulatory response to hypoventilation is aimed at eliminating carbon dioxide and maintaining oxygen delivery (DO(2)) by increasing cardiac output (CO). The hypothesis that this increase is more pronounced with xenon than with isoflurane anaesthesia was tested in pigs. METHODS: Twenty pigs received anaesthesia with xenon 0.55 MAC/remifentanil 0.5 microg kg(-1) min(-1) (group X, n=10) or isoflurane 0.55 MAC/remifentanil 0.5 microg kg(-1)min(-1) (group I, n=10). CO, heart rate (HR), mean arterial pressure (MAP) and left ventricular fractional area change (FAC) were measured at baseline, after 5 and 15 min of hypoventilation and after 5, 15 and 30 min of restored ventilation. RESULTS: CO increased by 10-20% with both anaesthetics, with an equivalent rise in HR, maintaining DO(2) in spite of a 20% reduction in arterial oxygen content. Decreased left ventricular (LV) afterload during hypoventilation increased FAC, and this was more marked with xenon (0.60-0.66, P<0.05 compared with baseline and isoflurane). This difference is attributed to negative inotropic effects of isoflurane. Increased pulmonary vascular resistance during hypoventilation was found with both anaesthetics. CONCLUSION: The cardiovascular effects observed in this model of moderate hypoventilation were sufficient to maintain DO(2). Although the haemodynamic response appeared more pronounced with xenon, differences were not clinically relevant. An increase in FAC with xenon is attributed to its lack of negative inotropic effects.

Analysis of Variance↗
PubMed2000

Cerebral oxygenation during hemorrhagic shock: perils of hyperventilation and the therapeutic potential of hypoventilation.

OBJECTIVES: Prophylactic hyperventilation of patients with head injuries worsens outcome, presumably by exacerbating tissue hypoxia. Oxygen tension in brain tissue (PbrO2) provides a direct measurement of cerebral metabolic substrate delivery and varies with changing end-tidal carbon dioxide tension (ETCO2) and mean arterial pressure. However, the effects of hyperventilation and hypoventilation on PbrO2 during hemorrhagic shock are not known. The aim of this study was to examine the effects of alteration in ventilation on PbrO2 in hemorrhaged swine. METHODS: Clark-type polarographic probes were inserted into the brain tissue of seven swine to measure PbrO2 directly. To examine the effects of alterations in ventilation on hemorrhage-induced hypotension, swine were hemorrhaged to 50% estimated blood volume and PbrO2 was monitored during hyperventilation (RR = 30) and hypoventilation (RR = 4). RESULTS: After the 50% hemorrhage, PbrO2 declined rapidly from 39.8 +/- 4.6 mm Hg to 11.4 +/- 2.2 mm Hg. Hyperventilation resulted in a further 56% mean decrease in PbrO2. Hypoventilation produced a 166% mean increase in PbrO2. These changes were significant (p = 0.001) for absolute and percentage differences from baseline. CONCLUSION: During hemorrhage, alterations in ventilation significantly changed PbrO2: hyperventilation increased brain-tissue hypoxia whereas hypoventilation alleviated it. This finding suggests that hyperventilation has deleterious effects on brain oxygenation in patients with hemorrhagic shock and those with head trauma. Conversely, hypoventilation with resultant hypercapnia may actually help resolve hemorrhagic shock-induced cerebral hypoxia.

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↗