Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 68-year-old man with severe dyspnea was admitted as an emergency case. He had no past history of any respiratory or neuromuscular diseases. Immediately after insufflation of oxygen, respiratory arrest occurred. The blood gas analysis showed hypoxemia and severe hypercapnia (PaO2; 32 mmHg, PaCO2; 127 mmHg). We diagnosed as CO2 narcosis, and he was treated with a respirator in the ICU. He showed nonflaccid bilateral diaphragmatic paralysis and muscle atrophy of the upper extremities. As the EMG showed giant spikes of neurogenic pattern, he was diagnosed as ALS. Weaning from the respirator failed because of his respiratory muscle fatigue. He was given rehabilitation during the day time and ventilatory support with the respirator during the night. We conclude that if we meet with an emergency patient with CO2 narcosis without any pulmonary disorder, we have to suspect neuromuscular diseases, e.q. ALS. In some of such cases, mechanical ventilation supports social rehabilitation.
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PMID:[A case of emergency admission for CO2 narcosis in a patient with amyotrophic lateral sclerosis]. 852 59

1. The role of supra-brainstem structures in the ventilatory response to inhaled CO2 is unknown. The present study uses positron emission tomography (PET), with infusion of H2(15)O, to measure changes in relative regional cerebral blood flow (rCBF) in order to identify sites of increased neuronal activation during CO2-stimulated breathing (CO2-SB) in awake man. 2. Five male volunteers were scanned during CO2-SB (mean +/- S.E.M.; end-tidal PCO2, 50.3 +/- 1.7 mmHg; respiratory frequency, 16.4 +/- 2.7 min-1; tidal volume, 1.8 +/- 0.2 l). As control, scans were performed during 'passive' isocapnic (elevated fraction of inspired CO2) positive pressure ventilation (end-tidal PCO2, 38.4 +/- 1.0 mmHg; respiratory frequency, 15.5 +/- 2.2 min-1; tidal volume, 1.6 +/- 0.2 l). With CO2-SB, all subjects reported dyspnoea. 3. The anatomical locations of the increases in relative rCBF (CO2-SB versus control) were obtained using magnetic resonance imaging. 4. Group analysis identified neuronal activation within the upper brainstem, midbrain and hypothalamus, thalamus, hippocampus and parahippocampus, fusiform gyrus, cingulate area, insula, frontal cortex, temporo-occipital cortex and parietal cortex. No neuronal activation was seen within the primary motor cortex (at sites previously shown to be associated with volitional breathing). 5. These results suggest neuronal activation within the limbic system; this activation may be important in the sensory and/or motor respiratory responses to hypercapnia in awake man.
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PMID:Evidence for limbic system activation during CO2-stimulated breathing in man. 856 67

We evaluated the use of a lateral thoracoscopic approach for lung reduction surgery in patients with diffuse emphysema. Sixty-seven patients with a mean age of 61.9 years underwent operation. Operative side was determined by preoperative imaging. The procedures were laser ablation in 10 patients and stapler resection in 57 patients. Ten patients, including six of the 10 patients in the laser-only group had poor outcome (death or hospitalization longer than 30 days), leading us to abandon the laser technique. Of the remaining 57 patients undergoing primary stapled resection, duration of chest tube placement averaged 13 days (range 3 to 53 days) with a mean hospital stay of 17 days (range 6 to 99 days). Seven patients required ventilation for longer than 72 hours, six patients underwent conversion of the procedure to open thoracotomy, four patients acquired arrhythmias, and three patients were treated for empyema. There was one early death (1.7%), from cardiopulmonary failure. Forty patients returned for 3-month evaluation. Significant (p < 0.0001) improvements were seen in forced vital capacity (2.69 L after vs 2.26 L before) and forced expiration volume in 1 second (1.04 L after vs 0.82 L before), with 25 of 40 patients (63%) showing an improvement of more than 20%. Lung volume measures, in particular residual volume, fell significantly. Arterial blood gas analysis revealed that carbon dioxide tension fell significantly in patients with preoperative hypercapnia (carbon dioxide tension > 45 mm Hg, p = 0.018). Six-minute walk test results improved (894 feet after vs 784 feet before, p = 0.002), and symptomatic benefit was confirmed by significant improvement in the dyspnea index. The combination of both hypercapnia and reduced single-breath diffusing capacity for carbon monoxide was significantly more frequent (p = 0.0026) and was 86% specific (5 of 6 patients) in predicting serious postoperative risk. We conclude that the lateral thoracoscopic surgical approach to diffuse emphysema offers significant improvement in pulmonary mechanics and functional impairment. Patients with a combination of hypercapnia and reduced single-breath diffusing capacity for carbon monoxide should not be considered for this procedure because of significant perioperative risk.
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PMID:Unilateral thoracoscopic surgical approach for diffuse emphysema. 858 1

There is intriguing evidence suggesting pathophysiologic relationships among dyspnea, hyperventilation, and panic anxiety. The symptoms of panic attacks and pulmonary disease overlap, so that panic anxiety can reflect underlying cardiopulmonary disease and dyspnea can reflect an underlying anxiety disorder. The pathogenesis of panic may be related to respiratory physiology by several mechanisms: the anxiogenic effects of hyperventilation, the catastrophic misinterpretation of respiratory symptoms, and/or a neurobiologic sensitivity to CO2, lactate, or other signals of suffocation. In a subset of patients with PD, incipient pulmonary dysfunction may also contribute to their anxiety symptoms. Patients with pulmonary disease, particularly those with obstructive lung disease, have a high rate of panic symptoms and PD. There is reason to believe that pulmonary disease constitutes a risk factor for the development of panic related to repeated experiences with dyspnea and life-threatening exacerbations of pulmonary dysfunction, repeated episodes of hypercapnia or hyperventilation, the use of anxiogenic medications, and the stress of coping with chronic disease. Panic in pulmonary patients may carry significant morbidity, including phobic avoidance of activity, overly aggressive treatment with anxiogenic medications, and more prolonged and frequent hospitalization. Successful treatment of panic in these patients can improve functional status and quality of life by relieving anxiety and dyspnea. Nonpharmacologic treatment of panic, including cognitive-behavioral approaches, can be useful in patients with concomitant respiratory disease. Sedating medications such as benzodiazepines should be used with caution in patients with pulmonary disease to avoid respiratory depression. Serotonergic antidepressants (SSRIs) and anxiolytics (buspirone) may be effective treatments for panic or generalized anxiety in pulmonary patients and have relatively little potential for significant adverse effects.
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PMID:Panic anxiety, dyspnea, and respiratory disease. Theoretical and clinical considerations. 868 Jul

Half of the patients admitted to intensive care units are elderly and may require mechanical ventilation for respiratory failure. Although age is not an independent factor for determining weaning outcomes, it may play a role. Elderly patients are predisposed to hypoxic-hypercapnia failure caused by age-related pulmonary changes and coexisting diseases. These age-related changes limit the respiratory reserve, which affects the body's ability to provide an adequate oxygen supply to meet the demand. The consequence is that during weaning there may be an imbalance between supply and demand and weaning failure may result. More research is needed regarding the weaning of elderly patients. Some specific areas that require further investigation are the relationship between age and dyspnea, the influence of age on weaning, and the relationship between age and the work of breathing.
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PMID:Failure to wean: exploring the influence of age-related pulmonary changes. 869 36

One hundred forty-one patients were prospectively enrolled in a study of contact-tip laser bullectomy at four institutions. Ninety-one have had both preoperative and postoperative testing at 3 months. Nonsmoking patients with disabling dyspnea at less than 50 yards and with a forced expiratory volume in 1 second of 35% or less were enrolled. Testing included formal pulmonary function tests, arterial blood gasses, computed tomographic scans, ventilation/perfusion scans, echocardiograms, electrocardiograms, 6-minute walk testing, transdiaphragmatic pressures, and quality of life and dyspnea index questionnaires. A modest 16% improvement was noted in forced expiratory volume in 1 second (0.69 to 0.80 L), and there was a 29% improvement in 6-minute walk distances (655.2 to 846.3 feet). Oxygen use was completely discontinued in 16%. Risk factors for mortality included age, 6-minute walk distances, low diffusing capacity for carbon monoxide, high carbon dioxide tension, and high base excess. Minor improvement was judged from the dyspnea index and the Medical Outcome Study Short Form-36. Preoperative predictors of good outcome included heterogeneous disease, lack of carbon dioxide retention, and no emaciation (weight < 40 kg). Comparison of our results with those in the literature suggests that the improvement seen with the contact neodymium:yttrium-aluminum-garnet laser is not as good as that provided by the stapled techniques for volume reduction.
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PMID:Thoracoscopic laser bullectomy: a prospective study with three-month results. 875 98

The objective of this study was to compare patient-ventilator interaction during pressure-support ventilation (PSV) and proportional-assist ventilation (PAV) in the course of increased ventilatory requirement obtained by adding a dead space in 12 patients on weaning from mechanical ventilation. With PSV, the level of unloading was provided by setting the inspiratory pressure at 20 and 10 cmH2O, whereas with PAV the level of unloading was at 80 and 40% of the elastic and resistive load. Hypercapnia increased (P < 0.001) tidal swing of esophageal pressure and pressure-time product per breath at both levels of PSV and PAV. During PSV, application of dead space increased ventilation (VE) during PSV (67 +/- 4 and 145 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001). This was due to a relevant increase in respiratory rate (48 +/- 4 and 103 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001), whereas the increase in tidal volume (VT) played a small role (13 +/- 1 and 21 +/- 2% during 20 and 10 cmH2O PSV, respectively, P < 0.001). With PAV, the increase in VE consequent to hypercapnia (27 +/- 3 and 64 +/- 4% during 80 and 40% PAV, respectively, P < 0.001) was related to the increase in VT (32 +/- 1 and 66 +/- 2% during 80 and 40% PAV, respectively, P < 0.001), respiratory rate remaining unchanged. The increase in pressure-time product per minute and per liter consequent to acute hypercapnia and the sense of breathlessness were significantly (P < 0.001) higher during PSV than during PAV. Our data show that, after hypercapnic stimulation of the respiratory drive, the capability to increase VE through changes in VT modulated by variations in inspiratory muscle effort is preserved only during PAV; the compensatory strategy used to increase VE during PSV requires greater muscle effort and causes more pronounced patient discomfort than during PAV.
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PMID:Patient-ventilator interaction during acute hypercapnia: pressure-support vs. proportional-assist ventilation. 882 95

A 61-year-old woman with chronic asthma sustained an episode of dyspnea and chest heaviness and was brought to the emergency department. Her examination revealed tachypnea, tachycardia, hypotension, and diffuse prolonged respiratory wheezing. Arterial blood gas analysis showed severe hypoxemia and hypercapnia. A 12-lead electrocardiogram showed marked, downsloping ST-segment depression, with deep, negative T waves in leads I, II, III, and aVF and precordial leads V3-V6. After 15 minutes of therapy with oxygen, beta-agonists, and corticosteroids, the electrocardiographic abnormalities subsided and 2 hours later they had disappeared. Subsequent coronary angiography and ventriculography revealed normal coronary arteries and good left ventricular ejection fraction. It is concluded that an acute asthmatic paroxysm may produce transient myocardial ischemia even with angiographically documented normal coronary arteries.
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PMID:Acute, reversible myocardial ischemia in a patient with an asthmatic attack. 891 9

Exercise rehabilitation programmes are increasingly recommended in young asthmatics, but it is unclear whether or not training should incorporate instructions on breathing pattern. In this study, we examined the effects of voluntarily decreasing breathing frequency on their ventilatory equivalents for oxygen and carbon dioxide (minute ventilation (V'E)/oxygen consumption (V'O2) and V'E/CO2 production (V'CO2), respectively), noninvasively determined physiological dead space/tidal volume (VD/VT) and dyspnoea. Fifteen young asthmatic subjects were assigned to two groups: low frequency breathing (LFB) and controls. They first underwent an exercise test at a cardiac frequency of 150 beats x min(-1). They were trained at this level for nine sessions. LFB subjects were instructed to decrease respiratory frequency by 40% during exercise. Control subjects received no instructions. A second test was then performed in the same conditions. LFB subjects decreased V'E/V'O2, V'E/V'CO2 and VD/VT by 22, 19 and 12%, respectively. Arterial oxygen saturation (Sa,O2) fell to 89+/-4% and end-tidal carbon dioxide tension (PET,CO2) rose to 6.5+/-0.7 kPa (49+/-5 mmHg). In controls, these variables were identical in the two tests. Dyspnoea was lower in the second test in all subjects. In conclusion, breathing pattern may be profoundly altered during exercise without concomitant increase in dyspnoea. However, directing breathing patterns for exercise rehabilitation requires an individual assessment of the desired pattern in order to prevent hypercapnia or hypoxia.
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PMID:Voluntary decrease in breathing frequency in exercising asthmatic subjects. 894 71

The purpose of this study is to examine the relationship between breathlessness and the ventilatory response to hypercapnia or hypoxia in patients with chronic obstructive pulmonary disease (COPD). Fifteen male patients (mean forced expiratory volume in one second (FEV1): 1.13 L) underwent tests to determine hyperoxic hypercapnic ventilatory response (HCVR) and isocapnic hypoxic ventilatory response (HVR) with simultaneous quantification of breathlessness by modified Borg scale. The ventilatory output was evaluated by the ratio of minute ventilation (V'E) divided by measured maximal voluntary ventilation (MVV). The magnitude of HCVR or HVR was assessed as the slope value of the V'E/MVV-end-tidal carbon dioxide pressure (PET,CO2) or arterial oxygen saturation (Sa,O2) regression line, respectively. The breathlessness during the tests was evaluated not only linearly in relation to V'E/MVV, but also at given levels of PET,CO2 or Sa,O2. The mean value of the breathlessness at two different levels of ventilation was greater during HVR than during HCVR, suggesting that hypoxia is dyspnogenic independently of ventilatory stimulation. The HCVR was inversely correlated with the breathlessness response to ventilation, while similar correlation was partly present for HVR. The HVR was positively correlated with the breathlessness at an Sa,O2 of 80%, whilst there was no such correlation between the HCVR and the breathlessness related to PET,CO2. Therefore, patients with a higher breathlessness related to increased ventilation had a lower HCVR and HVR, whilst those with a higher breathlessness with desaturation, which might include a direct influence of hypoxia, had a higher HVR. These findings suggest an interaction between ventilatory response and breathlessness during the test, which may partly include behavioural modulation of HCVR and HVR through the breathlessness in various ways, depending on the origin and nature of the sensation.
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PMID:Relationship between breathlessness and hypoxic and hypercapnic ventilatory response in patients with COPD. 894 82


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