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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors describe the application of NIV as a useful tool to correct hypercarbia, gas exchanges and to reduce the complications caused by mechanical ventilation with ETT in patients with acute exacerbation of COPD and acute asthma attack.
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PMID:[NIV in the treatment of acute exacerbation of COPD and status asthmaticus]. 1137 14

The term respiratory care has more than one meaning, referring both to a subject area within clinical medicine and to a distinct health care profession. In the light of several fundamental transformations of health care during the 20th century, this article reviews the history of respiratory care in both of these contexts and offers 10 predictions for the future: (1) Less focus on raising P(aO2) as a primary goal in managing patients with acute hypoxemic respiratory failure. (2) More attention to the adequacy of tissue oxygenation in such patients, irrespective of P(aO2), and the emergence of "permissive hypoxemia," analogous to permissive hypercapnia, in managing them. (3) Smarter monitors that display information less but process it more, while interacting directly with ventilators and other devices to modify therapeutic interventions. (4) Increased use of and expertise with noninvasive ventilation, with a corresponding decrease in intubations and complications, in treating patients with acute exacerbations of COPD. (5) Increased use of triage in the intensive care unit, including earlier determination of the appropriateness of maximal supportive intervention. (6) Greater use of protocols in patient assessment and management, in all clinical settings. (7) Increased awareness of, expertise in, and resources for palliative care, with a more active and acknowledged role for respiratory therapists. (8) Accelerating progress in smoking cessation and prevention, and also in early detection and intervention in COPD, led by the respiratory care profession. (9) An increasing presence and impact of respiratory therapists as coordinators and care givers in home care. (10) A continued and enlarging role for the journal Respiratory Care in disseminating research findings, clinical practice guidelines, protocols, and practical educational materials in all areas of the field.
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PMID:The future of respiratory care. 1171 25

Despite publication of several management guidelines for COPD, relatively little is known about standards of care in clinical practice. Data were collected on the management of 1400 cases of acute admission with Chronic Obstructive Pulmonary Disease in 38 UK hospitals to compare clinical practice against the recommended British Thoracic Society standards. Variation in the process of care between the different centres was analysed and a comparison of the management by respiratory specialists and nonrespiratory specialists made. There were large variations between centres for many of the variables studied. A forced expiratory volume in one second measurement was found in only 53% of cases. Of the investigations recommended in the acute management arterial blood gases were performed in 79% (interhospital range 40-100%) of admissions and oxygen was formally prescribed in only 64% (range 9-94%). Of those cases with acidosis and hypercapnia 35% had no further blood gas analysis and only 13% received ventilatory support. Long-term management was also deficient with 246 cases known to be severely hypoxic on admission yet two-thirds had no confirmation that oxygen levels had returned to levels above the requirements for long-term oxygen therapy. Only 30% of current smokers had cessation advice documented. To conclude, the median standards of care observed fell below those recommended by the guidelines. The lowest levels of performance were for patients not under the respiratory specialists, but specialists also have room for improvement. The substantial variation in the process of care between hospitals is strong evidence that it is possible for other centres with poorer performance to improve their levels of care.
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PMID:Audit of acute admissions of COPD: standards of care and management in the hospital setting. 1140 9

The host of chronic respiratory abnormalities responsible for an abnormal hematosis or for a handicap can be termed generically as chronic respiratory insufficiency. Hypoxemia can be the consequence of perturbations of oxygen transfer (fibrosis), of abnormal ventilation-perfusion ratios (venous admixture, chronic obstructive pulmonary disease [COPD]), or of hypoventilation (neuromuscular diseases). Hypercapnia can stem from hypoventilation (neuromuscular diseases), or from abnormal ventilation-perfusion ratios (dead space effect) (COPD). An imbalance between the capacity of the respiratory muscle to produce negative inspiratory pressures and the load they are faced with is a source of hypercapnia, and of dyspnoea and handicap independently of hematosis (COPD, neuromuscular diseases). The effects of hypoxemia on cellular functions make chronic respiratory insufficiency a systemic disease.
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PMID:[Physiopathology of chronic respiratory insufficiency]. 1146 4

This issue of Sleep and Breathing presents a section on sleep in COPD, a widespread disease consuming many health resources which is often diagnosed so late that little chance of reversibility remains. The early detection of the warning clinical signs can include sleep studies, mainly in the presence of arterial carbon dioxide levels higher than expected from pulmonary function tests. Two of the articles deal with hypercapnia and nocturnal hypoventilation in COPD; the third underlines the impact of tobacco smoking on snoring and on oxygen availability to tissues, showing a poor reliability of pulse oximetry in subjects with heavy smoking habits.
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PMID:Sleep disordered breathing and COPD. 1191 57

Extreme mountain climbers and patients with stable but severe ventilatory insufficiency (e.g. obesitas hypoventilation-syndrome, scoliosis) sometimes experience a state of severe hypoxemia without any or only mild subjective disturbances. Organ failure is never observed in these periods. On the other hand there are two well documented studies concerning long term oxygen therapy (LTOT) that have shown in hypoxemic COPD-patients (pO 2 lower then 55 mm Hg) a doubling the life expectancy under oxygen. This contradiction can be elucidated if the influence of oxygen on the ventilation is taken into account. These study patients treated with LTOT all had more or less hypercapnia (hypoventilation) due to an overload of their respiratory pump. Oxygen reduces the ventilation (seen as hypercapnia) which leads to an unloading of the respiratory muscles. Later studies to LTOT found a positive correlation between the extent of stable hypercapnia and life expectancy. In this article the physiopathologic background of this findings are discussed. The main parameter of the regulator for the oxygen transport is not pO 2 but the oxygen content. The oxygen content multiplied by cardiac output determines the extent of oxygen delivery. Many regulatory systems (e.g. polyglobuly or expression of oxygen resistant isoenzymes of the respiratory chain) are involved to compensate the hypoxemia associated with hypoventilation which prevents an organ threatening hypoxia. This pathophysiologic finding has important impact on intensive care medicine, which usually takes only pO 2 into account for therapeutic decisions (e. g. high FiO 2 and high pressure support). This sometimes leads to "overtreatment", with possible harm to the patient.
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PMID:[Overestimation of hypoxemia]. 1214 Jul 93

Hypercapnia has been accepted during nasal intermittent positive pressure ventilation (nIPPV) and during subsequent spontaneous breathing in patients with chronic hypercapnic respiratory failure (HRF) due to COPD. We tested the hypothesis that nIPPV aimed at normalizing PaCO2 will reduce PaCO2 during subsequent spontaneous breathing. For that purpose 14 consecutive inpatients (age 61.4 +/- 9.9 years) with chronic HRF due to COPD were established on passive pressure-controlled nIPPV in a stepwise approach. Assisted ventilation with supplemental oxygen to reach normoxemia was started followed by passive ventilation with a stepwise increment in the inspiratory pressure and finally by a stepwise increase in the respiratory rate to establish normocapnia. Baseline pulmonary function parameters were: FEV1 0.97 +/- 0.43 l, PaCO2 59.5 +/- 8.4 mmHg, PaO2 49.9 +/- 7.8 mmHg, HCO3- 35.6 +/- 5.2 mmol/l, pH 7.39 +/- 0.04. Normoxemia as well as normocapnia was thus established by decreasing PaCO2 by 19.5 +/- 7.0 mmHg during nIPPV within 8.8 +/- 3.8 days (P < 0.001) (inspiratory pressure 29.8 +/- 3.8 mmHg, respiratory rate 22.9 +/- 1.9 BPM). Spontaneous PaCO2 measured 4 h after cessation of nIPPV decreased to 46.0 +/- 5.5 mmHg (P < 0.001), and HCO3- decreased to 27.2 +/- 3.0 mmol/l (P < 0.001). At 6 months of follow-up, II patients continued nIPPV with stable blood gases and with a decrease of P0.1/Plmax from 9.4 +/- 4.3% to 5.9 +/- 2.0% (P < 0.005). In conclusion, normalization of PaCO2 by passive nIPPV in patients with HRF due to COPD is possible and leads to a significant reduction of PaCO2 during subsequent spontaneous breathing and is associated with improved parameters of respiratory muscle function.
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PMID:Normocapnia during nIPPV in chronic hypercapnic COPD reduces subsequent spontaneous PaCO2. 1219 37

To study the value of low volume ventilation in chronic obstructive lung disease (COPD) with Type II respiratory failure, 35 patients were divided into two groups at random. The tidal volume of regular volume ventilation group was 12-14 ml.kg-1 and that of low volume ventilation group was 6-8 ml.kg-1. Some indexes of airway pressures and blood gases were recorded and those of cardiovascular function were monitored continuously. The results were that compared to the normal volume ventilation group, the actual ventilation in liters per minute was lower obviously, the expiratory time longer, the incidence rate of lung barotrauma lower, peak inspiratory pressure, end-inspiratory-pressure, and internal positive-end-expiratory pressure smaller, and side-effect on hemodynamics less in the low volume group. The results suggest that low volume ventilation with permissive hypercapnia is better than normal volume ventilation in COPD.
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PMID:[Low volume mechanical ventilation in the treatment of patients with chronic obstructive lung diseases with type II respiratory failure]. 1221 48

V(A)/Q mismatching and load/capacity imbalance are the major physiologic determinants of chronic respiratory failure. The former underlies lung failure and the consequent development of hypoxemia. The latter causes chronic ventilatory failure and hypercapnia. This is the consequence of an inefficient breathing pattern with lower VT and higher respiratory rate, probably due to the "wise choice" of preventing excessive inspiratory effort and eventually respiratory muscle fatigue. In many disorders, V(A)/Q mismatching and the load/capacity imbalance coexist, particularly in COPD, where the interplay between the two pathophysiologically represents the advanced stage of the disease. In other disorders, one of the two mechanisms prevails; for example, V(A)/Q mismatching in pure lung diseases, and chest wall mechanics in thoracic disorders. This has important therapeutic implications because oxygen administration can relieve hypoxemia, whereas mechanical ventilation can prevent excessive hypercapnia and respiratory acidosis. Although the role of oxygen therapy is well established, the role of chronic mechanical ventilation is still a matter of debate, particularly in COPD. A major task for future research is to achieve the best possible understanding of the pathophysiologic factors predisposing to chronic ventilatory failure, to prevent the progression of the respiratory diseases to the stage when chronic respiratory failure eventually develops.
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PMID:Physiologic factors predisposing to chronic respiratory failure. 1248 63

Long-term MV, delivered by way of a tracheostomy or noninvasive mask, often is indicated in patients with restrictive or neuromuscular pulmonary diseases and occasionally in patients with severe obstructive hypercapnic respiratory failure. Regardless of the mode of ventilation, respiratory physiology seems to be significantly impacted in these patients. Although the effects of ventilation can be unpredictable, they often seem to be favorable. Selected patients can develop increased sensitivity to hypercapnia, with subsequent improvements in blood gas tensions and decreased pulmonary artery pressures, which result in augmented cardiac function and greater tolerance to exercise. The patient-ventilator interaction, mode of ventilation, and degree of support should be considered when managing these patients. For some patients, particularly patients with fibrotic lung disease or COPD, chronic MV likely does not alter pathophysiology or improve prognosis.
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PMID:Physiologic responses to long-term ventilation. 1248 66


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