Hypercapnia
Article Abstract:
Hypercapnia is an excess of the gas carbon dioxide (CO2) in the blood, caused by many diseases. Carbon dioxide is normally produced in the body and eliminated by the lungs. The efficiency of the lung structure itself and the amount of air exchanged within the structures of the lungs, will determine the percent of CO2 remaining in the blood. Poor ventilation-profusion, the breathing in and exchange of air within the lungs, results in hypercapnia. Hypercapnia can be the result of altered CO2 production. This can be caused by an increase in metabolic activity in the body, fever or disease. Problems with air exchange can be caused by diseases that compromise lung functioning. Weak breathing muscles, fatigue, and poor functioning of the diaphragm muscle, which works with the lungs during breathing, can cause poor mechanical breathing and reduce the lungs' ability to remove CO2. Changes in the respiratory control system, which controls the breathing muscles, can also cause hypercapnia. Obese people frequently have poor breathing muscle function. Chronic obstructive pulmonary disease (COPD), bronchitis and emphysema are all lung diseases which result in decreased airflow from diseased lung tissue and poor lung function, causing a build-up of CO2 in the blood. An alteration in breathing pattern can also contribute to hypercapnia. Excess CO2 in the blood can cause problems in the kidneys, heart and central nervous system, because excess CO2 means that less oxygen is available in the blood. Treatment should reduce the amount of CO2 from all causes. Drugs can be given to dilate the bronchial tubes, decrease the work of breathing, improve the functioning of the diaphragm muscle, stimulate and improve ventilation. Oxygen supplements can also be given.
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 1989
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Recent advances in pulmonary medicine
Article Abstract:
Pulmonary medicine is moving beyond the assessment and treatment of patients with lung disease. Understanding the molecular basis of diseases such as cystic fibrosis, alpha1-antitrypsin deficiency, obstructive lung disease and asthma can lead to new treatments. Cystic fibrosis (CF) is caused by a gene defect that causes thick secretions in the lungs. Knowledge of the defect may open the door to gene therapy for CF. Enzyme therapy can be used to treat alpha1-antitrypsin deficiency, which causes a breakdown of elastic lung tissue. Inhaled beta-agonists and other bronchodilators are the treatment of choice for COPD, and oxygen can be beneficial. Asthma is a reversible inflammation and obstruction of the airway that is best treated with inhaled corticosteroids or beta-agonists. Computed tomography (CT), magnetic resonance imaging (MRI) and pulse oximetry have revolutionized the diagnosis of lung disease.
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 1993
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Weaning from ventilatory support
Article Abstract:
Weaning patients from a ventilator is the process by which doctors determine whether patients can breathe on their own so they can be removed from the machine. Many weaning methods involve adjusting the ventilator so that the machine supplies less ventilation and the patient supplies more of the respiratory effort. However, a 1995 study found that patients could be weaned more quickly if given a once-daily trial of spontaneous breathing rather than a gradual drawdown of ventilator support. This technique may not be inherently faster, but may simply allow doctors to determine sooner whether patients on a ventilator can breathe on their own. However, a trial of spontaneous breathing may be dangerous; consequently, the patient should be closely watched.
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 1995
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