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

In humans, attenuating carotid chemoreceptor activity by hyperoxia does not alter arterial PCO2 (PaCO2) during submaximal exercise, yet a transient hypercapnia occurs in carotid chemoreceptor-resected (CBR) asthmatic subjects during submaximal exercise. We hypothesized that this difference was due to asthma and not CBR causing the abnormal response. Accordingly, we determined the temporal pattern of PaCO2 during mild and moderate exercise in chemoreceptor-intact asthmatic (n = 10) and nonasthmatic subjects (n = 10). We also hypothesized that hyperoxia alters PaCO2 during exercise if exercise already has disrupted PaCO2 homeostasis. Accordingly, we studied, during exercise, asthmatic subjects while hyperoxic; nonasthmatic subjects during loaded breathing of room air, which increased PaCO2; and nonasthmatic subjects during loaded breathing while hyperoxic. While breathing room air, neither asthmatic nor nonasthmatic subjects maintained arterial isocapnia during exercise. An increase in PaCO2 between rest and exercise and between mild exercise and 1st min of moderate exercise was greater in asthmatic than in nonasthmatic subjects (P < 0.05). In six asthmatic subjects that were hypercapnic breathing room air during exercise, hypercapnia was accentuated by hyperoxia. The ventilatory load in nonasthmatic subjects resulted in a work load-dependent hypercapnia (P < 0.01) accentuated (P < 0.01) by hyperoxia. We conclude that normally in humans the carotid chemoreceptors contribute minimally to the hyperpnea of submaximal exercise. However, when PaCO2 is increased from resting values during exercise, then the chemoreceptors serve to augment ventilation and thereby minimize the hypercapnia.
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PMID:Effect of asthma and ventilatory loading on arterial PCO2 of humans during submaximal exercise. 771 39

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.
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PMID:Update on the management of status asthmaticus. 881 99

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

On admission to intensive care units, the acid-base profile in acute severe asthma appears to be more diverse than previously. Especially a mixed or less frequently metabolic acidosis is eventually observed, which is not always caused by elevated lactate. On the other hand, hyperlactatemia is actually rather common, not necessarily accompanied by acidosis. This finding is as a rule related to massive doses of beta 2 adrenergic agents given parenterally: subsequent elevated lactate is in no way a marker of cellular hypoxia and has no pejorative meaning in this event. Hypercapnia with severe respiratory acidosis implies less and less mechanical ventilation; however, when mandatory, it has to be carried out using permissive hypercapnia, giving more favorable outcome while lowering side-effects.
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PMID:[Acidosis in severe acute asthma]. 895 66

Experimental and clinical evidence has led to a revision of conventional techniques used for mechanical ventilation in the treatment of respiratory failure due to severe asthma and acute respiratory distress syndrome. A common feature in these two clinical situations is the heterogeneous nature of the lesions, causing mechanical alterations which vary from one region to another. Thus the tidal volume is not equally distributed throughout the lungs and can lead to overdistension in some regions or functional exclusion in others. Hyperinflation then exposes the patient to barotrauma, cardiocirculatory and/or alveolocapillary complications. Controlled hypoventilation-or permissive hypercapnia-is a new approach aimed at preventing complications by supplying adequate oxygen while accepting or provoking a certain degree of hypercapnia by alveolar hypoventilation. The technique is based on restricting tidal volume and respiratory rate as long as is necessary to recover more favorable mechanical conditions. Results obtained with this method have been convincing for the treatment of decompensated asthma but preliminary data obtained in acute respiratory distress syndrome remain to be validated.
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PMID:[Permissive hypercapnia. From choice to unavoidable decision]. 895 67

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.
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PMID:Critical care management of the asthmatic patient. 952 98

Despite improved understanding of the basic mechanisms underlying asthma, morbidity and mortality remain high, especially in the "inner cities." The treatment of choice in status asthmaticus includes high doses of inhaled beta 2-agonists, systemic corticosteroids, and supplemental oxygen. The roles of theophylline and anticholinergics remain controversial, although in general these agents appear to add little to the bronchodilator effect of inhaled beta-agonists in most patients. Anti-leukotriene medications have not yet been evaluated in acute asthma. Other therapies, such as magnesium sulfate and heliox, have their advocates but are not recommended as part of routine care. If pharmacological therapy does not reverse severe airflow obstruction in the asthmatic attack, mechanical ventilation may be temporarily required. Based on our current understanding of ventilator-induced lung injury, optimal ventilation of asthmatic patients avoids excessive lung inflation by limiting minute ventilation and prolonging expiratory time, despite consequent hypercapnia. Unless respiratory function is extremely unstable, the use of paralytic agents is discouraged because of the increased risk of intensive care myopathy. Patients who have suffered respiratory failure due to asthma are at increased risk for subsequent death due to asthma (14% mortality at 3 years) and should receive very close medical follow-up. In general, severe asthmatic attacks can best be prevented by early intervention in the outpatient setting. In the words of Dr. Thomas Petty, "... the best treatment of status asthmaticus is to treat it three days before it occurs".
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PMID:Medical and ventilatory management of status asthmaticus. 953 66

Morbidity and mortality derived from asthma continue to be a main public health problem in many countries, in spite of the advances in the knowledge on the disease and its treatment. There are several risk factors for asthma attack which have to be considered in the management of patients in order to prevent exacerbations and mortality. Smooth bronchial muscle constriction and inflammation with oedema of the bronchial wall are the facts that cause airway flow and resistance disturbances, with hyperinflation, leading to a bigger respiratory work. On the other hand, the bronchial obstruction leads to a ventilation-perfusion disequilibrium and hypoxia. At the beginning of the process there is hypocarbia, but when the attack progresses muscle fatigue happens, and retention of CO2, being a sing of alarm (predictive of respiratory failure) a normal and rising PaCO2. The evaluation of an acute asthmatic patient should accomplish a clinical and objective assessment (peak flow rate and saturation of O2), in order to classify the crisis in: mild, moderate or severe. Managing acute asthmatic patient includes: oxygen, bronchodilator ss2 agonists at high and even continuous doses and systemic corticosteroids to prevent the progression and to control inflammation. These procedures should be promptly instituted. Although there is less evidence on their beneficial effects other measures as intravenous aminophylline, nebulized anticholynergics, magnesium sulphate and intravenous ss2 agonists may be used when the conventional therapy is not quickly successful and the patient is in a critical situation, at a real risk of respiratory failure, and in order to avoid mechanical ventilation. If this is finally instituted, controlled hypoventilation with permissive hypercarbia is now recommended, to avoid barotrauma, which used to be a frequent complication when more aggressive attitude was the rule. Interaction between paralytic agents and corticosteroids may produce a miopathy, so the recommendation now is to try not to use paralytic agents, even with profound sedation of needed. Sixty four patients were treated on 77 occasions in the Pediatric Intensive Care Unit of our hospital. They were 0,5 to 13,9 years old, being 50% less than 5 years old. It was the first attack in 9 (14%) patients. The standard management consisted of oxygen, frequently or continuously nebulized salbutamol and intravenous methylprednisolone (1 to 6 mg/kg/day). Furthermore nebulized ipratropium bromide was administered 58 times (75%), as well as intravenous aminophylline 69 (89%), intravenous salbutamol 23 (30%), magnesium sulphate 16 (21%) and ketamine 10 (13%). Antibiotics were given 22 times (29%). Two 15 month old infants received mechanical ventilation in three occasions, and relevant complications happened (pneumothorax and myopathy, and pneumomediastinum and bronchiolitis obliterans respectively). Fifty six patients have been followed for a period of 3 to 110 months (median 48 months), and 16 (29%) have needed high doses (equal to or move than 800 mcg of budesonide or equivalent). There are data on lung function in 36 of them, FEV1 is normal (> 85% of predicted, between 86 and 127) in 26 (78%) and < 85% (65 to 84%) of predicted in 8 (22%) FEV1 rises more than 15% (16 to 23%) in four patients after the inhalation of a ss2 agonist. Inhaled anesthetic agents and heliox have been used in some pediatric cases. After a severe asthma attack the strategy of management should be reviewed, as well as the possible risk factors.
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PMID:[Round Table: Severe asthma in pediatrics: treatment of acute crises]. 1035 7

Permissive hypercapnia (acceptance of raised concentrations of carbon dioxide in mechanically ventilated patients) may be associated with increased survival as a result of less ventilator-associated lung injury. Conversely, hypocapnia is associated with many acute illnesses (eg, asthma, systemic inflammatory response syndrome, pulmonary oedema), and is thought to reflect underlying hyperventilation. Accumulating clinical and basic scientific evidence points to an active role for carbon dioxide in organ injury, in which raised concentrations of carbon dioxide are protective, and low concentrations are injurious. We hypothesise that therapeutic hypercapnia might be tested in severely ill patients to see whether supplemental carbon dioxide could reduce the adverse effects of hypocapnia and promote the beneficial effects of hypercapnia. Such an approach could also expand our understanding of the pathogenesis of disorders in which hypocapnia is a constitutive element.
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PMID:Carbon dioxide and the critically ill--too little of a good thing? 1052 Jun 49

The ventilatory drive is affected by several factors such as chemosensitivity, basal arterial oxygen or carbon dioxide tension, mechanical impedance, and respiratory muscle dysfunction. Blunted ventilatory drive or a decrease in the perception of dyspnea in bronchial asthma and chronic obstructive pulmonary disease (COPD) could lead to a decrease in the alarm reaction to dangerous situations such as severe airway obstruction, severe hypoxemia, or severe hypercapnia. This could delay management and treatment, causing an increase in the morbidity and mortality of patients with bronchial asthma and COPD. The ventilatory drive to chemical stimuli can be altered by a beta-2-agonist, oxygen administration; and lung volume reduction, and an increased dyspnea sensation may be improved by corticosteroid, chest wall vibration, or lung volume reduction. The ventilatory drive has been found to play a key role in determining the severity of asthma and COPD.
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PMID:Role of ventilatory drive in asthma and chronic obstructive pulmonary disease. 1057 Jul 33


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