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

The multiple chemical sensitivities syndrome (MCS) and other chronic syndromes causing fatigue, headache and other protean CNS symptoms without observable signs, are proposed to result from hypoxia/hypercapnia (H/H) due to disturbed breathing. The concept is explained in terms of sleep apnea (SA), although H/H could result from causes other than SA. Reasons for considering this etiologic linkage are as follows: 1. MCS symptoms resemble those of SA. 2. The only physical signs associated with MCS (upper airway inflammation and obstruction) can aggravate SA. 3. The only neuropsychiatric finding common among MCS symptomatics, reduced verbal recall, is associated with SA. 4. Many MCS symptomatics attribute onset of their condition to a pesticide or solvent exposure. Solvent neurotoxicity may cause cacosmia, a symptom of MCS and SA. 5. Improved upper airway patency, a first-line therapy in SA, may improve symptoms in some MCS-like conditions. Implications for diagnosis and treatment of MCS are discussed.
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PMID:Chemical sensitivity and fatigue syndromes from hypoxia/hypercapnia. 1085 79

Decrease of respiratory muscle capacities in neuromuscular disease can lead to chronic respiratory failure with permanent alveolar hypoventilation. Respiratory centers elaborate a strategy of breathing dedicated to prevent overt respiratory muscles fatigue. This strategy may worsen chronic hypercapnia. During sleep, ventilation decreases because a lessening in respiratory centers function. During NREM sleep hypoventilation is only an exacerbation of what is seen during wakefulness. During REM sleep, atonia worsens much more hypoventilation particularly when diaphragmatic function is impaired. The effects of atonia are amplified by a very low reactivity of respiratory centers. Nocturnal mechanical ventilation improves nocturnal hypoventilation and daytime arterial blood gases (ABG). Mechanism of improvement in ABG and how nocturnal hypoventilation and diurnal hypoventilation interact, are still a matter of debate.
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PMID:Nocturnal hypoventilation in chronic respiratory failure (CRF) due to neuromuscular disease. 1089 4

Once it is decided that the patient in distress requires tracheal intubation, the primary goal is to secure the airway as quickly and safely as possible to assure adequate oxygenation and ventilation. The clinician should quickly review the patient's history, physical examination findings, and laboratory data to determine the presence of cardiovascular disease, assess intravascular volume status, and formulate a plan for induction of anesthesia. The stresses of hypoxia, hypercarbia, acidosis, and extreme fatigue result in near-maximal sympathetic outflow that is manifest as tachycardia, labile blood pressure, and increased myocardial contractility. The astute clinician should anticipate that the tachycardia and hypertension associated with laryngoscopy and tracheal intubation is followed by a period of hypotension. This postintubation hypotension results from the acute marked attenuation of the sympathetic tone associated with resolution of hypoxia and hypercarbia, direct drug-induced negative inotropic effect, and vasodilation. The decrease in sympathetic vascular tone may result in hypotension by exacerbating the decrease in cardiac preload and afterload from hypovolemia. In addition, the use of positive pressure ventilation and positive end-expiratory pressure (PEEP) in these hypovolemic patients will further decrease ventricular preload by impeding venous return, leading to profound hypotension. Several pharmacologic agents are required to treat effectively the hemodynamic perturbations associated with induction, laryngoscopy, and tracheal intubation. Most sedative hypnotic agents that are administered for induction provide minimal to no analgesia. Patients are most often given a combination of drugs to provide adequate sedation, analgesia to blunt the noxious stimuli, and muscle relaxation to facilitate the laryngoscopy. The major challenge is to choose a combination of drugs that at the appropriate doses, effectively blunt the responses to intubation without contributing to postlaryngoscopy hypotension. One can use several strategies to accomplish these goals; administration of a narcotic analgesic before induction decreases the dose of induction agent and can attenuate the sympathetic response to intubation. Because of the prevalence of cardiovascular disease and hypovolemia in this population of patients, all chosen drugs should have minimal negative effect on cardiac function and patients with hypovolemia should be hydrated. Most clinical studies have been performed in hemodynamically stable patients, so the routine dosages of sedative hypnotics should be reduced substantially and titrated to effect. An additional strategy is to treat significant hemodynamic perturbations with vasopressors, vasodilators, short-acting selective beta-1 blockers, and inotropic agents. The choice of vasoactive agent depends on the magnitude of the hemodynamic response and the presence of specific underlying cardiovascular pathology.
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PMID:Emergent management of the airway. New pharmacology and the control of comorbidities in cardiac disease, ischemia, and valvular heart disease. 1094 81

Acute Respiratory Failure (ARF) results in an inability to maintain gas exchange at a rate commensurate with the demands of the body and results in hypoxemia and/or hypercarbia, the mechanisms of which may be different. Hypoxemia commonly occurs due to Ventilation Perfusion (V/Q) mismatching, intrapulmonary shunt, diffusion defect or hypoventilation. Hypercarpnic respiratory failure may also be multifactorial but is usually due to inhibited central respiratory drive or inefficient respiratory muscle pump. Hypercapnia may occur in upper and lower airways obstruction, respiratory muscle fatigue and occasionally due to excess CO2 production (burns and excessive glucose administration). Issues in management centre around assessment of severity, determining the need for intervention, establishing diagnosis and etiology and institution of specific treatment. Diagnosis of respiratory failure may be made clinically and confirmed by blood gas analysis. Calculation of oxygenation indices will delineate extent of hypoxemia. When evaluating a child with respiratory failure, one should be aware that a child with prominent respiratory symptoms may have non-respiratory disease (i.e. metabolic acidosis, DKA) and conversely, advanced respiratory failure may be present in a child with no respiratory distress (central hypoventilation secondary to drugs, infection) careful assessment of history, complete physical examination and evaluation of lab parameters may clarify the diagnosis. Serial assessment of sensorium, respiratory symptoms, ABG and response to treatment will provide valuable clues to determine the need for intervention. Oxygen, like any drug, must be administered in a prescribed dose, only when indicated with the potential risks borne in mind. A variety of oxygen delivery devices are available; which ever device is used, the resulting FiO2 and devisable end points must be clearly determined. Hazards of oxygen therapy range from retinal damage in premature infants, damage to the alveolar capillary membrane with resultant hypoxemia) atelectasis and decreased mucociliary activity.
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PMID:Acute respiratory failure and oxygen therapy. 1133 23

Chronic obstructive pulmonary disease (COPD) is a leading cause of death, and constitutes a major medical and an increasing economic problem for acute and long term care. A low level of irreversible airway obstruction when in stable condition, hypercapnia, hypoxia, the presence of comorbid heart disease, right ventricular failure, and low serum albumin are the main factors related to risk of exacerbations. Bronchial infections, bronchospasm, left ventricular failure, pneumonia, pneumothorax and thromboembolism are described as the most frequent relapsing causes of COPD. During exacerbation, the inflammatory process, the ventilation/perfusion (V'A/Q') mismatching, an increased airflow resistance and dynamic hyperinflation (PEEPidyn) expose the respiratory muscles to the risk of fatigue, eventually leading to ventilatory pump failure and rising hypercapnia. Prevention of exacerbations and subsequent hospitalisations may be obtained with careful rehabilitation programs, a strict drug protocol, long term oxygen therapy and sometimes using home noninvasive mechanical ventilation (NMV). During exacerbation proper management of infection and lung mechanics derangement has to be adopted using an accurate assessment of severity and standardized treatment protocols. Patient history and examination and functional tests are beneficial to decide how and where to treat these patients. Mechanical ventilation (possibly noninvasive) may be required to reverse the acute episode. The aims of all these procedures remain: i) to prolong length and quality of life; ii) to save costs. Both hospital and post-discharge mortality of exacerbated COPD remain high while quality of life appears to be poor. Future studies will elucidate the relation between number and severity of exacerbations and prognosis.
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PMID:Exacerbations of COPD: predictive factors, treatment and outcome. 1149 3

Daytime complaints like fatigue, sleepiness and cognitive dysfunction in neuromuscular disease can be due to nocturnal hypercapnia and hypoxemia. Daytime respiratory diagnostics does not reflect sleep disordered breathing. Nocturnal pulse oxymetry and capnography were performed in 11 patients (15-75 years old) with different slowly progressive neuromuscular diseases. Only four patients complained of dyspnea. Pulmonary function was abnormal in three patients. Blood gas samples showed a hypoxemia in three patients. Pulse oxymetry results were pathological in six patients. Nine patients presented abnormal capnographies. According to these results either nocturnal oxygen application was initiated or ventilatory parameters were modified. Daytime symptoms and muscular strength improved markedly. Capnography and pulse oxymetry should be performed during the course of neuromuscular disease to detect respiratory insufficiency. Capnography seems to be a more sensitive indicator for respiratory impairment especially when artificial ventilation has been initiated.
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PMID:Respiratory monitoring in neuromuscular disease - capnography as an additional tool? 1151 50

The exercising Thoroughbred horse (TB) is capable of exceptional cardiopulmonary performance. However, because the ventilatory equivalent for O2 (VE/VO2) does not increase above the gas exchange threshold (Tge), hypercapnia and hypoxemia accompany intense exercise in the TB compared with humans, in whom VE/VO2 increases during supra-Tge work, which both removes the CO2 produced by the HCO buffering of lactic acid and prevents arterial partial pressure of CO2 (PaCO2) from rising. We used breath-by-breath techniques to analyze the relationship between CO2 output (VCO2) and VO2 [V-slope lactate threshold (LT) estimation] during an incremental test to fatigue (7 to approximately 15 m/s; 1 m x s(-1) x min(-1)) in six TB. Peak blood lactate increased to 29.2 +/- 1.9 mM/l. However, as neither VE/VO2 nor VE/VCO2 increased, PaCO2 increased to 56.6 +/- 2.3 Torr at peak VO2 (VO2 max). Despite the presence of a relative hypoventilation (i.e., no increase in VE/VO2 or VE/VCO2), a distinct Tge was evidenced at 62.6 +/- 2.7% VO2 max. Tge occurred at a significantly higher (P < 0.05) percentage of VO2 max than the lactate (45.1 +/- 5.0%) or pH (47.4 +/- 6.6%) but not the bicarbonate (65.3 +/- 6.6%) threshold. In addition, PaCO2 was elevated significantly only at a workload > Tge. Thus, in marked contrast to healthy humans, pronounced V-slope (increase VCO2/VO2) behavior occurs in TB concomitant with elevated PaCO2 and without evidence of a ventilatory threshold.
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PMID:Mechanistic basis for the gas exchange threshold in Thoroughbred horses. 1189 16

Severe asthma, although difficult to define, includes all cases of difficult/therapy-resistant disease of all age groups and bears the largest part of morbidity and mortality from asthma. Acute, severe asthma, status asthmaticus, is the more or less rapid but severe asthmatic exacerbation that may not respond to the usual medical treatment. The narrowing of airways causes ventilation perfusion imbalance, lung hyperinflation, and increased work of breathing that may lead to ventilatory muscle fatigue and life-threatening respiratory failure. Treatment for acute, severe asthma includes the administration of oxygen, beta2-agonists (by continuous or repetitive nebulisation), and systemic corticosteroids. Subcutaneous administration of epinephrine or terbutaline should be considered in patients not responding adequately to continuous nebulisation, in those unable to cooperate, and in intubated patients not responding to inhaled therapy. The exact time to intubate a patient in status asthmaticus is based mainly on clinical judgment, but intubation should not be delayed once it is deemed necessary. Mechanical ventilation in status asthmaticus supports gas-exchange and unloads ventilatory muscles until aggressive medical treatment improves the functional status of the patient. Patients intubated and mechanically ventilated should be appropriately sedated, but paralytic agents should be avoided. Permissive hypercapnia, increase in expiratory time, and promotion of patient-ventilator synchronism are the mainstay in mechanical ventilation of status asthmaticus. Close monitoring of the patient's condition is necessary to obviate complications and to identify the appropriate time for weaning. Finally, after successful treatment and prior to discharge, a careful strategy for prevention of subsequent asthma attacks is imperative.
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PMID:Clinical review: severe asthma. 1194 Feb 64

The factors that may modulate ventilatory muscle fatigue during exercise are controversial. In this study the contribution of acidosis to exercise-induced diaphragmatic fatigue was investigated, using measurements of the twitch mouth pressure response (tw,Pmo) to cervical magnetic stimulation. After learning sessions, 14 healthy subjects performed two cycling tests (at 60% of maximal aerobic power for 16 min), one while breathing spontaneously (mean minute ventilation (V'E) 67.9 L x min(-1)) and the other while hypoventilating voluntarily (mean V'E 53.8 L x min(-1)). Exercise was voluntarily set at a moderate power to avoid a fatiguing effect of exercise per se. As compared with spontaneous breathing (SB), voluntary hypoventilation (VHV) significantly increased mean carbon dioxide tension in arterial blood (Pa,CO2) (51 mmHg versus 41 mmHg) and significantly decreased arterial pH (7.28 versus 7.34). After 10 min of SB test, tw,Pmo was unchanged compared to the baseline value (19.1 versus 18.5 cmH2O) whereas tw,Pmo fell significantly as compared to baseline (17.1 versus 18.5 cmH2O) and to SB (17.1 versus 19.1 cmH2O) after the VHV test. The results of this study suggest that exposure to hypercapnia may impair respiratory muscle function. This impairment could be more clinically relevant in patients with chronic obstructive lung disease.
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PMID:Contribution of respiratory acidosis to diaphragmatic fatigue at exercise. 1210 60

About 80,000 polio survivors are still living 40 years after the last polio epidemics in Germany. Of these 40-70% have developed the so called post-polio syndrome (PPS) decades after the infection. The main symptoms of PPS are decreasing strength in voluntary muscles, pain and fatigue which occur spontaneously but may also be induced by physical stress and general illness. We report the case of a 79-year-old male who developed hypercapnia due to ventilatory failure which necessitated reintubation several times after cholecystectomy. The medical history revealed that he had had poliomyelitis at the age of 8 years. There was only a slight residual handicap from this infection which included mild pareses of the left limbs but had remained stable for about 70 years. Electromyography revealed signs of chronic neurogenic changes in muscles of the left upper limb as well as in the pectoralis major. The diagnostic criteria of a post-polio syndrome were fulfilled and other neuromuscular diseases were excluded. The patient could be discharged from intensive care only after treatment by intermittent positive pressure ventilation via a facial mask. This case report shows that even patients who have a mild handicap after poliomyelitis can develop weaning problems. A PPS can exacerbate with inclusion of respiratory muscles in critically ill patients.
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PMID:[40 years after the last polio epidemic. Postpolio syndrome as a cause of "weaning failure"]. 1212 9


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