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

Weaning failure is, unfortunately, a rather common phenomenon for mechanically-ventilated patients (especially those with chronic obstructive pulmonary disease (COPD)), and the respiratory muscles play a pivotal role in its development. Weaning fails whenever an imbalance exists between the ventilatory needs and the neurocardiorespiratory capacity. This can happen if there is an increase in the energy demands of the respiratory muscles, a decrease in the energy available, a decrease in neuromuscular competence, or if the respiratory muscles pose an impediment to the heart and blood flow. The imbalance created will lead to weaning failure through the development of respiratory muscle fatigue, hypercapnia, dyspnoea, anxiety and organ dysfunction.
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PMID:Respiratory muscles and weaning failure. 894 90

Pulmonary hyperinflation is usually defined as an abnormal increase in functional residual capacity, i.e. lung volume at the end of tidal expiration. As such, it is virtually universal in patients with symptomatic diffuse airway obstruction. Hyperinflation inferred from a standard chest radiograph implies an increase in total lung capacity. The relaxation volume of the respiratory system (Vr) increases in patients with chronic airway disease as a result of changes in the elastic properties of the lungs and chest wall. In addition, a variable degree of dynamic hyperinflation may be present. This results from the onset of inspiration before lung volume has fallen to Vr. Dynamic hyperinflation is frequently present at rest in patients with moderate-to-severe airway obstruction, and it increases further on exercise, thereby increasing the mechanical load on the inspiratory muscles and at the same time reducing their mechanical advantage. Important clinical consequences and associations of hyperinflation include: distortions of chest wall motion; impaired inspiratory muscle function; increased oxygen cost of breathing; greater likelihood of hypercapnia; impaired exercise performance; and greater severity of breathlessness. The symptomatic improvement after treatment with a bronchodilator may be due, in part, to lessening of hyperinflation.
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PMID:Pulmonary hyperinflation a clinical overview. 898 Sep 82

A 13-year-old boy with juvenile-onset acid alpha glucosidase deficiency was reported. Proximal muscle weakness including respiratory muscles and scoliosis progressed since nine year of age. He developed nocturnal dyspnea and daytime somnolence at age 13. His arterial blood gas analysis showed hypoxemia (PO2 54.1 mmHg) and hypercapnia (PCO2 72.3 mmHg), and spirometry showed significantly decreased vital capacity (% VC 21%). He was treated with nocturnal NIPPV employing a device for delivering bilevel positive airway pressure (Bi-PAP). Nocturnal dyspnea and daytime somnolence rapidly disappeared with nocturnal ventilatory support. Daytime arterial PO2 and PCO2 improved after the therapy, namely 74.8 mmHg and 64.1 mmHg respectively. We conclude that NIPPV is a noninvasive and effective therapy for respiratory failure in patients with chronic progressive neuromuscular disorder including acid alpha glucosidase deficiency.
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PMID:[Chronic respiratory failure in a case with juvenile-onset acid alpha-glucosidase deficiency; successful therapy with nasal intermittent positive pressure ventilation (NIPPV)]. 898 97

Complications may occur when nutritional support is administered either parenterally or enterally. Inappropriate nutritional formulas with high carbohydrate loads can precipitate respiratory failure in patients with compromised lung function, induce respiratory distress which manifests as dyspnea and tachypnea in an originally normal lung condition, produce hypercapnic acidosis in mechanically ventilated patients with chronic obstructive pulmonary disease (COPD) as well as patients recovering from acute respiratory distress syndrome (ARDS) without chronic lung disease, or result in difficult weaning. Hypercaloric mixed substrates administered either parenterally or enterally can also have profound impacts on gas exchange and energy expenditure. This report describes a patient who experienced exacerbation of respiratory distress and hypercapnic acidosis during recovery from septic ARDS as the result of a nutritionally-related increase in CO2 production. As carbohydrate calories were decreased, CO2 production diminished and the hypercapnia was resolved. The importance of indirect calorimetry cannot be overemphasized during tailoring of nutritional support for the critically ill patients.
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PMID:Hypercapnic respiratory acidosis precipitated by hypercaloric carbohydrate infusion in resolving septic acute respiratory distress syndrome: a case report. 903 53

Most of the lower limb surgeries are done under spinal anesthesia. This 21 year-old male had undergone open reduction with interlocking nail for his right femoral fracture and was scheduled for removal of interlocking nail. Spinal anesthesia was performed and a sensory block up to T8 level was achieved. During removing of the nail, the patient complained of chest pain, dyspnea and headache. Consequently, tachycardia and hypotension were observed. Then he coughed up pink frothy sputum. Ephedrine 5 mg was given to raise his blood pressure. About 3 min later, he recovered from the hypotension. Arterial blood gas analysis showed hypoxemia and hypercapnia. After endotracheal intubation, he was sent to surgical intensive care unit. In surgical intensive care unit, fat globules in urine, anemia and thrombocytopenia were noted. Chest roentgenogram showed patchy pulmonary infiltrates in the left lower lobe. A pulmonary artery catheter was inserted for pulmonary measurement, which read pulmonary artery pressure 45/28 mmHg, wedge pressure 14 mmHg, and cardiac output was 5-34 L/min. Supportive treatment which included steroid therapy, and O2 therapy with positive end-expiratory pressure was initiated under the impression of pulmonary embolism. The course in surgical ICU was uneventful and he left there three days later and was discharged on the fifth hospitalization day.
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PMID:[Removal of femoral interlocking nail-induced pulmonary embolism under spinal anesthesia--a case report]. 908 55

Sleep has a physiological influence on respiration, which can have major adverse effects on gas exchange in patients with respiratory insufficiency. These effects relate largely to a reduction in various stimulant inputs to the brainstem respiratory centre. Conditions that may be associated with sleep-related respiratory insufficiency range from pulmonary disorders (such as chronic obstructive pulmonary disease (COPD)), to central respiratory insufficiency (such as central alveolar hypoventilation), neurological and neuromuscular disorders (such as polio and muscular dystrophy), and thoracic cage disorders (such as kyphoscoliosis). All these conditions have in common the finding of hypoxaemia and hypercapnia, which become more pronounced during sleep. The relative hypoventilation, which is common to each condition, is due to varying combinations of an inadequate respiratory drive and an increase in the work of breathing. Management of respiratory insufficiency during sleep should be directed first at optimizing the underlying disorder, then at correcting hypoxaemia with controlled low-flow supplemental oxygen. Pharmacological therapy may be effective in some instances, but the choice of agent varies with the underlying disorder. Assisted ventilation is an important part of the management of advanced cases, and the recent development of intermittent positive pressure ventilation by nasal mask (NIPPV) has been an important advance in this area. Use of NIPPV during the night is associated with beneficial effects during the day, particularly improved awake gas exchange and respiratory muscle strength, in addition to less dyspnoea and improved quality of life. Electrophrenic pacing of the diaphragm is helpful in highly selected cases, particularly patients with central respiratory insufficiency and high quadriplegia, but is frequently complicated by the development of obstructive sleep apnoea.
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PMID:Impact of sleep in respiratory failure. 915 Mar 36

We tried to verify, in a clinical setting, the hypothesis that enhanced perception of dyspnoea (PD) and increased respiratory drive (RD): 1) relate to each other; and 2) elicit an integrated response that leads to a decrease in RD and tidal volume (VT) aimed at minimizing PD. In 34 patients with chronic obstructive pulmonary disease (COPD), dyspnoea was graded on a four-point scale after a Medical Research Council (MRC) questionnaire concerning respiratory symptoms. Patients were divided into four groups according to the dyspnoea score. Pulmonary volumes, arterial blood gases, VT, respiratory frequency (fR), inspiratory time (tI), expiratory time (tE), maximal inspiratory pressure (MIP), and maximal expiratory pressure (MEP) were measured. RD was also assessed in terms both of mouth occlusion pressure (P0.1) and electromyographic (EMG) activity of the respiratory muscles. Increase in dyspnoea rating was associated with decrease in vital capacity (VC), forced expiratory volume in one second (FEV1), MIP, VT and tI; and increase in arterial carbon dioxide tension (Pa,CO2), P0.1, and EMG (analysis of variance (ANOVA) and Bonferroni's test). A rapid and shallow pattern of breathing (RSB) characterized the group with the highest dyspnoea rating. Stepwise multiple regression analysis showed that: 1) tI and FEV1 accounted for a substantial proportion of the variability in VT and tI, respectively; 2) VT and MIP, together, predicted a substantial proportion of the variability in Pa,CO2 (r2 = 0.50). We conclude that, in patients with chronic obstructive pulmonary disease clinical rating of dyspnoea appears to be associated with muscle weakness and increase in respiratory drive. The increased respiratory drive is modulated into a rapid and shallow pattern of breathing, which leads to hypercapnia.
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PMID:Breathlessness and control of breathing in patients with COPD. 915 15

Noninvasive mechanical ventilation (NMV) now represents the first step in the management of acute on chronic respiratory failure (A/CRF). During the last 5 yrs, many studies have confirmed the feasibility of NMV in an acute setting, either by facial or nasal interface, used in addition to volumetric or barometric respirators, to manage A/CRF. The best indications for NMV are slowly progressive A/CRF, frequently represented by chronic obstructive pulmonary disease (COPD), or restrictive pulmonary disease. The criteria to initiate NMV in such patients are worsening of respiratory status and arterial blood gas (ABG) values, with increased hypoxia, hypercapnia and respiratory acidosis, despite optimal management with medication, physiotherapy and oxygen therapy. Respiratory encephalopathy is not an absolute contraindication; however, bronchial hypersecretion indicates that care is needed under NMV. Invasive mechanical ventilation with endotracheal (ET) intubation is discussed in the case of failure of NMV, when clinical status and ABG values worsen in spite of it. The signal for ET intubation is then obvious, represented by severe dyspnoea leading to respiratory pauses or arrest, severe cyanosis, and signs of haemodynamic instability. Despite immediate evidence of ominous cardiorespiratory inefficiency, ET intubation may be delayed and often avoided with the help of NMV. Criteria should be studied to identify guidelines for cessation of NMV, in order not to continue with the technique too long considering the safety of the patient. Indications for NMV in other kinds of ARF have received less study and are more controversial.
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PMID:Noninvasive mechanical ventilation and acute respiratory failure: indications and limitations. 915 23

Vibration of chest wall inspiratory muscles during inspiration (in-phase) reduces breathlessness associated with hypercapnia and resistive loading in normal subjects and in patients with chronic obstructive pulmonary disease (COPD) at rest. To evaluate further the effect of chest wall vibration on breathlessness ("breathing discomfort") in patients, we studied 10 subjects 52 to 79 yr of age with severe dyspnea (mean FEV1, 0.75 L, 27% predicted). On a single day, we used two separate stimuli to produce mild to moderate breathlessness (BR): Protocol 1, steady-state hypercapnia; Protocol 2, exercise with a lower extremity ergometer. During each protocol, we applied in-phase chest wall vibration (CW) randomly alternating with one of two controls: deltoid vibration (DV) or no vibration (NV). During hypercapnia, CW significantly reduced BR (DV, 2.9 +/- 2.1; CW, 2.3 +/- 1.4; p < 0.05; NV, 3.3 +/- 2.1; CW, 2.6 +/- 2.0; p < 0.01) without significant changes in ventilation. During exercise, CW did not significantly alter BR relative to controls. These findings may be explained by the effect of vibration on the sense of respiratory effort and/or by improvement of the match between efferent motor commands and afferent information from the respiratory system. The lack of effect during exercise on BR suggests there may be a "therapeutic window" or range of conditions within which CW is effective in reducing dyspnea in patients with COPD.
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PMID:Effect of chest wall vibration on dyspnea during hypercapnia and exercise in chronic obstructive pulmonary disease. 915 56

Patients in hypercapnic respiratory failure have got a poor prognosis. The recognition of pathophysiological mechanisms is required in order to choose adequate therapy. During the past years it has been shown that pathological respiratory events during sleep occur early in the disease process and that blood gas changes are usually most pronounced during sleep. Minute ventilation and functional residual capacity (FRC) decrease during sleep even in normal subjects and upper airway resistance increases markedly. PO2 slightly decreases and paCO2 increases. In most patients with hypercapnic respiratory failure episodes of marked hypoxemia and hypercapnia occur, mainly during REM sleep. Suggested pathomechanisms are worsening ventilation-/perfusion mismatching, impaired respiratory muscle function and a reduction in ventilatory drive, the latter two being of major importance. The relation between load and capacity is shifted towards an increased load and ventilatory drive is decreased at the same time. Therapeutic strategies that reduce the load of the respiratory pump, increase minute ventilation and prevent sleep related hypoventilation, thus noninvasive ventilation should be used. Symptoms of hypercapnic respiratory failure are often unspecific. Dyspnea, headache and awakening from sleep with dyspnea are often reported. Signs of right heart failure will be present in advanced disease stages. Early diagnosis and treatment provided, noninvasive ventilation achieves excellent improvement of both quality of life and life expectancy, especially if the primary disease progress is not rapidly progressive.
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PMID:[Pathophysiology and clinical aspects of global respiratory insufficiency]. 923 56


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