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

When a patient with chronic obstructive pulmonary disease (COPD) requires medical therapy for systemic hypertension, a number of special considerations may affect the choice of antihypertensive drug and subsequent management. Thiazide diuretics have no adverse effect on airway function and are the agents of choice for initial therapy. beta-Antagonists are usually considered first-line agents in antihypertensive therapy, but even relatively cardioselective ones may increase airway resistance in patients with obstructive lung diseases, and they should be used with caution, if at all, in such patients. Although potassium-wasting diuretics are the preferred agents for treating hypertension in patients with COPD, they may worsen carbon dioxide retention in hypoventilating patients and potentiate hypokalemia in those receiving corticosteroids. In addition, beta-agonists may substantially lower serum potassium levels in patients already rendered hypokalemic by diuretics. Patients with COPD receiving potassium-wasting diuretics who have chronic respiratory acidosis or are receiving corticosteroids or beta-agonists should undergo close monitoring of electrolyte levels and be considered for therapy with potassium supplements or, preferably, potassium-sparing agents.
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PMID:Fluid and electrolyte considerations in diuretic therapy for hypertensive patients with chronic obstructive pulmonary disease. 286 47

Bicarbonate reabsorption by the immature kidney in response to acute acid-base changes was assessed in 50 anesthetized newborn rabbits before the end of nephrogenesis. The normal newborn rabbit (age 5-12 days) is in a state of hypochloremic metabolic alkalosis (PHCO3-, 31.9 +/- 0.6 mmol/l; PCl-, 83.1 +/- 1.0) and excretes a hypertonic (Uosmol = 578 +/- 41 mosmol/kgH2O), alkaline (UpH = 7.40 +/- 0.15) urine containing 50 +/- 9 mmol/l Cl- and 13 +/- 4 mmol/l Na+. The alkalosis is probably generated by an alkaline load contained in the mother's milk and maintained by a state of chloride wasting and volume contraction. In this alkalotic model, bicarbonate reabsorption, expressed per milliliter glomerular filtration rate (GFR), correlates positively with arterial CO2 pressure (PaCO2). The ability of the immature kidney to reclaim filtered bicarbonate in response to an elevation of the plasma carbon dioxide tension remains unlimited up to PaCO2 of 110 mmHg (y = 20.7 + 0.15 x, r = 0.82, P less than 0.001). Hypercapnia is associated with a marked fall in GFR, so that the positive correlation between bicarbonate reabsorption and PaCO2 vanishes when the bicarbonate reabsorption rate is expressed in absolute terms. Bicarbonate reabsorption is strongly dependent on the filtered load during both acutely induced metabolic acidosis and alkalosis. The acid-base state of the newborn rabbit is in sharp contrast with that of most animal species, and the renal handling of bicarbonate as a function of GFR does not show signs of tubular immaturity.
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PMID:Bicarbonate reabsorption by the kidney of the newborn rabbit. 291 64

A 52-year-old woman presented with increasing pain, weakness, and paraesthesiae of four months' duration in the lower limbs. She suffered from chronic obstructive airways disease and hypertension. Neurological examination revealed wasting of the quadriceps muscles, weakness of the lower limbs, and absent ankle jerks. The sensory examination was normal. Full blood count, ESR, biochemical, immunological, and viral studies, urinary heavy metal assays, and cerebrospinal fluid examination were normal. Nerve conduction studies were consistent with a sensorimotor neuropathy, and electromyographic sampling was consistent with acute denervation. A sural nerve biopsy showed axonal degeneration and segmental demyelination. One month after admission, she developed carbon dioxide retention. Her weakness spread to affect the upper limbs, and she could not be resuscitated after a cardiac arrest three months after admission. General autopsy examination revealed bronchopneumonia. Neuropathological examination showed a lymphocytic infiltrate in the nerve roots of the cauda equina, the lumbosacral plexus, and the sural and vagal nerves. Increased cellularity and collagen were evident in these nerves. A diagnosis of chronic inflammatory polyneuropathy was made. The neuropathology of this entity is discussed.
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PMID:Neuropathological findings in a case of chronic inflammatory polyneuropathy. 384 15

In many patients with neuromuscular diseases, respiratory failure is mainly caused by alveolar hypoventilation in their terminal stages. Malnutrition is one of the common and serious problems in patients with chronic respiratory failure. Energy consumption for breathing is remarkably high in respiratory compromised patients, causing subsequent increase of total energy expenditure. However, most patients have limited capacity of oral intake. Nutritional depletion is associated with wasting of respiratory muscles, impairment of respiratory drive, alteration of respiratory pattern, and pathological change of pulmonary parenchyma. These indicate that nutritional and ventilatory support is very important in these patients. However, overfeeding also may have detrimental influence on respiratory failure. We experienced a Duchenne muscular dystrophy (DMD) patient on noninvasive positive pressure ventilation (NIPPV) who developed hypercapnia after total parenteral nutrition (TPN). Analysis of clinical course of this patient revealed that there is a significant correlation between PaCO2 and caloric intake. Excess carbohydrate intake can precipitate fat synthesis which induces over-production of carbon dioxide (CO2). Since NIPPV doesn't have a closed circuit, there are some difficulties in respiratory management, such as air leakage to stomach and mouth, and airway obstruction. Failure to optimize NIPPV setting against increased CO2 load might cause hypercapnia in this patient. These suggest that evaluation of energy expenditure and design of nutritional program are essential to avoid hypercapnia due to nutritional support.
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PMID:[Excess caloric intake induced severe hypercapnia in a patient with Duchenne muscular dystrophy on noninvansive positive pressure ventilation]. 1007 34

Important features of both stable and acute exacerbation of chronic obstructive pulmonary disease (COPD) are skeletal muscle weakness and wasting. Limb muscle dysfunction during an exacerbation has been linked to various adverse outcomes, including prolonged hospitalization, readmission, and mortality. The contributing factors leading to muscle dysfunction are similar to those seen in stable COPD: disuse, nutrition/energy balance, hypercapnia, hypoxemia, electrolyte derangements, inflammation, and drugs (i.e., glucocorticoids). These factors may be the trigger for a downstream cascade of local inflammatory changes, pathway process alterations, and structural degradation. Ultimately, the clinical effects can be wide ranging and include reduced limb muscle strength. Current therapies, such as pulmonary/physical rehabilitation, have limited impact because of low participation rates. Recently, novel drugs have been developed in similar disorders, and learnings from these studies can be used as a foundation to facilitate discovery in patients hospitalized with a COPD exacerbation. Nevertheless, investigators should approach this patient population with knowledge of the limitations of each intervention. In this Concise Clinical Review, we provide an overview of acute muscle dysfunction in patients hospitalized with acute exacerbation of COPD and a strategic approach to drug development in this setting.
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PMID:Deterioration of Limb Muscle Function during Acute Exacerbation of Chronic Obstructive Pulmonary Disease. 2906 60