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Query: UMLS:C0020440 (
hypercapnia
)
7,939
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The objective of this study was to retrospectively review the medical records of 38 consecutive admissions to the medical intensive care unit of a tertiary-care university hospital of patients with severe asthma, and to determine the clinical characteristics of these patients, treatment regimens, and ultimate outcome. The 38 patients presented with severe asthma accompanied by hypoxemia,
hypercapnia
(mean pCO2 of 54.3 +/- 4.5 mm Hg), and decreased peak flow rates (125.5 +/- 12.4 L/min). The patients spent a mean of 60.1 +/- 9.7 hr in the medical intensive care unit. Seventeen of the 38 patients required intubation and mechanical ventilation. Overall, there were no deaths or significant complications. All 38 patients were discharged from the hospital. We conclude that severe, life-threatening asthma can be appropriately managed in the medical intensive care unit with a low incidence of complications and death. Prolonged mechanical ventilation is rarely required and most patients respond while the relatively simple management strategies.
J
Asthma
1995
PMID:Clinical features, management, and outcome of patients with severe asthma admitted to the intensive care unit. 755 78
Arterial blood gas data were correlated with clinical variables including patients' perception of dyspnea and spirometry in 79 episodes of acute asthma attacks. Among several variables that showed univariate significance with severity, only subjective degree of dyspnea rated on a modified Borg scale (MBS) remained predictive to discriminate the presence or absence of hypoxia/
hypercapnia
in multivariate analyses. MBS alone could predict the arterial blood gas status with accuracy of approximately 75%. Therefore, patients' sensation of dyspnea seemed to be an important factor in the evaluation of acute asthma in an emergency room.
J
Asthma
1994
PMID:Clinical features to predict hypoxia and/or hypercapnia in acute asthma attacks. 792 36
Asthma
is a common and debilitating problem in children. Its many costs to society include morbidity, hospitalization and treatment expenses, and a rising mortality rate. This paper examines recent trends in therapy for status asthmaticus. Oxygen, inhaled beta-adrenergic agonists, and corticosteroids remain the cornerstones of therapy for the child with a severe exacerbation of asthma. Ipratropium bromide provides additional bronchodilatation in the patient who does not respond to standard therapy. Theophylline may have a role in chronic outpatient management of asthma, but the data supporting the addition of this medication in acute therapy for status asthmaticus are inconclusive. Antibiotics are only indicated in children with asthma complicated by infection, such as sinusitis or pneumonia. Magnesium sulfate and heliox may have a role in helping the asthmatic child who is critically ill and for whom other interventions have failed. Mechanical ventilation has many complications. The concept of permissive
hypercapnia
may be important in limiting barotrauma. Prevention of exacerbations of asthma include limiting environmental exposure to allergens and tobacco, using corticosteroids, and reinforcing compliance with therapy.
...
PMID:Update on the management of status asthmaticus. 881 99
The incidence and severity of asthma continue to increase despite advances in therapy. Two types of severe asthma exacerbations have been described: "sudden onset" and "slow onset." Beta-adrenergic agonists and corticosteroids are still the mainstay of therapy in the intensive care unit.
Hypercapnic
hypoventilation is advocated as a mode of mechanical ventilation to maintain oxygenation while minimizing barotrauma. Sedating and paralytic agents must be used with caution to prevent complications such as myopathy, which may occur with prolonged use of these agents. Future avenues of study could include the use of leukotriene and platelet-activating factor inhibitors.
Asthma
management guidelines should be practiced to prevent worsening of bronchospasm to the point of severe exacerbation.
...
PMID:Critical care management of the asthmatic patient. 952 98
Asthma
and chronic obstructive pulmonary diseases (COPD) lead to functional obstruction of airways, identified by increased inspiratory and expiratory resistances. Increased expiratory resistances cause, in turn, a reduction in expiratory flow. The analysis of flow-volume loops shows that, as the disease progresses, the flow generated during expiration of a tidal volume becomes very close to the flow generated during forced maximal expiration. In such condition, where there is little or no reserve of expiratory flow, higher tidal volumes need to be reached in order to increase the expiratory flow, and hyperinflation inevitably occurs. Hyperinflation, a key feature in COPD pathophysiology, is generated by two mechanisms: reduction of elastic recoil of the lung (static hyperinflation) and interruption of expiration at lung volumes still higher than FRC, due to reduction of expiratory flow (dynamic hyperinflation). When dynamic hyperinflation occurs, a residual positive pressure remains in the alveoli, which is defined as intrinsic positive end-expiratory pressure (PEEPi). Hyperinflation carries several consequences: 1) Respiratory mechanics: at lung volumes close to total lung capacity, lung compliance is physiologically reduced, and elastic work required to generate the same inspiratory volume is therefore increased; 2) Respiratory muscles: contractile properties of diaphragm deteriorate when the dome is pushed downward by an increased lung volume, inspiration is mainly performed by inspiratory muscles, and expiration becomes active; 3) Circulation: pulmonary vascular resistances increase due to compression exerted by hyperinflation on alveolar vessels and to hypoxic vasoconstriction; right ventricle afterload increases and right sided hypertrophy and dilation ensue; left ventricular afterload may increase due to increased negative intrapleural pressure which translates into an increased transmural pressure which needs to be overcome by ventricular contraction. Ventilatory support of COPD patients should decrease work of breathing and improve gas exchange without increasing hyperinflation. This target can be achieved during assisted ventilation by applying a positive pressure both during inspiration and expiration; the level of PEEP should equal PEEPi. During mechanical ventilation in sedated paralyzed patients hyperinflation should be limited by decreasing minute volume and by increasing expiratory time, eventually choosing controlled
hypercapnia
.
...
PMID:[Physiopathology of acute respiratory failure in COPD and asthma]. 1137 10
Asthma
is a common and potentially serious condition complicating pregnancy. However, the literature available on the management of severe asthma in pregnancy is limited. We describe two episodes of respiratory failure due to asthma in pregnant women and discuss their management in the context of a review of the literature. In both patients, adequate oxygenation was maintained by using controlled hypoventilation with a permissive
hypercapnia
strategy. Both patients received aggressive steroid therapy, aerosolized bronchodilators, sedation, and paralysis. Aggressive asthma treatment as in a nongravid female is recommended.
J
Asthma
2005 Apr
PMID:Ventilator strategy for status asthmaticus in pregnancy: a case-based review. 1596 70
Several studies have demonstrated impaired control of ventilation in some patients with near-fatal asthma (NFA). The objective of our study was to determine a possible relationship between alexithymia (a cognitive processing disorder), control of ventilation, and breathlessness perception in patients who had an NFA attack. We analyzed data from 100 subjects: 50 with NFA, 25 asthmatics without NFA, and 25 non-asthmatic controls. Ventilatory responses to hypoxia and
hypercapnia
were measured by the rebreathing technique in terms of slope of ventilation and mouth occlusion pressure (P0.1). Breathlessness perception was assessed with the Borg scale and alexithymia with the Toronto Alexithymia Scale (TAS). No statistical differences were observed between groups in breathlessness perception and ventilatory responses. The mean (SD) TAS score of 63.6 (14.9) in the NFA group was significantly higher than the score of 56.4 (12.1) in the non-asthmatic group (p = 0.007). More subjects with alexithymia were identified in the NFA group (24%) than in the non-NFA group (12%) or the non-asthmatic control group (12%). Although the presence of alexithymia did not correlate with poor ventilatory responses or breathlessness perception, it was associated with a larger number of previous hospitalisations: 6.2 (8.1) in the NFA group and 2.8 (4.8) in the non-NFA group (p = 0.036). In conclusion, the prevalence of alexithymia is higher among NFA patients than among asthmatics who have not experienced NFA attacks. Neither altered breathlessness perception nor ventilatory response to hypoxia seems to play a role in NFA, although alexithymia may favor poor clinical control.
J
Asthma
2006 Oct
PMID:Control of ventilation, breathlessness perception and alexithymia in near-fatal asthma. 1705 Feb 32
Asthma
is a common chronic respiratory disorder with relatively good outcomes in the majority of patients with appropriate maintenance therapy. However, in a small minority, patients can experience severe asthma with respiratory failure and
hypercapnia
, necessitating intensive care unit admission.
Hypercapnia
occurs due to alveolar hypoventilation and insufficient removal of carbon dioxide (CO
2
) from the blood. Although mild
hypercapnia
is generally well tolerated in patients with asthma, there is accumulating evidence that elevated levels of CO
2
can act as a gaso-signaling molecule, triggering deleterious effects in various organs such as the lung, skeletal muscles and the innate immune system. Here, we review recent advances on pathophysiological response to
hypercapnia
and discuss potential detrimental effects of
hypercapnia
in patients with asthma.
...
PMID:Hypercapnia: An Aggravating Factor in Asthma. 3302 86