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

In order to describe the outcomes of patients hospitalized with an acute exacerbation of severe chronic obstructive pulmonary disease (COPD) and determine the relationship between patient characteristics and length of survival, we studied a prospective cohort of 1,016 adult patients from five hospitals who were admitted with an exacerbation of COPD and a PaCO2 of 50 mm Hg or more. Patient characteristics and acute physiology were determined. Outcomes were evaluated over a 6 mo period. Although only 11% of the patients died during the index hospital stay, the 60-d, 180-d, 1-yr, and 2-yr mortality was high (20%, 33%, 43%, and 49%, respectively). The median cost of the index hospital stay was $7,100 ($4,100 to $16,000; interquartile range). The median length of the index hospital stay was 9 d (5 to 15 d). After discharge, 446 patients were readmitted 754 times in the next 6 mo. At 6 mo, only 26% of the cohort were both alive and able to report a good, very good, or excellent quality of life. Survival time was independently related to severity of illness, body mass index (BMI), age, prior functional status, PaO2/FI(O2), congestive heart failure, serum albumin, and the presence of cor pulmonale. Patients and caregivers should be aware of the likelihood of poor outcomes following hospitalization for exacerbation of COPD associated with hypercarbia.
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PMID:Outcomes following acute exacerbation of severe chronic obstructive lung disease. The SUPPORT investigators (Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments) 888 92

A central apnea is a disorder characterized by apneic events during sleep with no associated ventilatory effort. Central sleep apnea syndrome is characterized by repeated apneas during sleep resulting from loss of respiratory effort. Although the etiology of central apnea remains obscure in most cases, current investigations into breathing control system during sleep and association with certain diseases have pointed out possible mechanisms. Ventilation during sleep is highly dependent on the nonbehavioral control system. As a result, any diseases affecting this control system could influence the breathing patterns while the patient is asleep. As our results show, most patients with central sleep apnea and without congestive heart failure had quantifiable abnormalities like diminished carbon dioxide response curves. Neurological diseases affecting the brainstem are able to produce breathing pattern disorders in sleep. Well-known neurological diseases such as arteriosclerosis in the elderly, infarctions, tumors, hemorrhage, accidents with damage of this region, encephalitis, poliomyelitis or other infectious diseases may cause central apnea during sleep, even if in wakefulness no abnormalities of breathing patterns are present. Apneas cause hypoxemia, hypercapnia and increased sympathicotonia. This may result in development of pulmonary artery hypertension or systemic hypertension. Published results demonstrate that medical treatment is ineffective in these patients. Implantation of a diaphragm pacing device is an invasive measure, the efficacy of the diaphragm pacing has not been proven by long-term trials, however. Mechanical ventilation was shown to be the most efficient treatment. A therapeutic procedure using a timed n-BiPAP device is able to normalize blood gases during sleep. The n-BiPAP prevented the development of severe pulmonary artery hypertension during sleep.
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PMID:Central sleep apnea. 904 68

Because of similar physiological changes such as increased left ventricular (LV) afterload and sympathetic tone, an exaggerated depression in cardiac output (CO) could be expected in patients with coexisting obstructive sleep apnea and congestive heart failure (CHF). To determine cardiovascular effects and mechanisms of periodic obstructive apnea in the presence of CHF, 11 sedated and chronically instrumented pigs with CHF (rapid pacing) were tested with upper airway occlusion under room air breathing (RA), O(2) breathing (O2), and room air breathing after hexamethonium (Hex). All conditions led to large negative swings in intrathoracic pressure (-30 to -39 Torr) and hypercapnia (PCO(2) approximately 60 Torr), and RA and Hex also caused hypoxia (to approximately 42 Torr). Relative to baseline, RA increased mean arterial pressure (from 97.5 +/- 5.0 to 107.3 +/- 5.7 Torr, P < 0.01), systemic vascular resistance, LV end-diastolic pressure, and LV end-systolic length while it decreased CO (from 2.17 +/- 0.27 to 1.52 +/- 0.31 l/min, P < 0.01), stroke volume (SV; from 23.5 +/- 2.4 to 16.0 +/- 4.0 ml, P < 0.01), and LV end-diastolic length (LVEDL). O2 and Hex decreased mean arterial pressure [from 102.3 +/- 4.1 to 16.0 +/- 4.0 Torr (P < 0.01) with O2 and from 86.0 +/- 8.5 to 78.1 +/- 8.7 Torr (P < 0.05) with Hex] and blunted the reduction in CO [from 2.09 +/- 0.15 to 1.78 +/- 0.18 l/ml for O2 and from 2.91 +/- 0.43 to 2.50 +/- 0.35 l/ml for Hex (both P < 0.05)] and SV. However, the reduction in LVEDL and LV end-diastolic pressure was the same as with RA. There was no change in systemic vascular resistance and LVEDL during O2 and Hex relative to baseline. In the CHF pigs during apnea, there was an exaggerated reduction in CO and SV relative to our previously published data from normal sedated pigs under similar conditions. The primary difference between CHF (present study) and the normal animals is that, in addition to increased LV afterload, there was a decrease in LV preload in CHF contributing to SV depression not seen in normal animals. The decrease in LV preload during apneas in CHF may be related to effects of ventricular interdependence.
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PMID:Hemodynamic effects of periodic obstructive apneas in sedated pigs with congestive heart failure. 1071 Apr 3

Obstructive sleep apnoea is a disease of increasing importance because of its neurocognitive and cardiovascular sequelae. Abnormalities in the anatomy of the pharynx, the physiology of the upper airway muscle dilator, and the stability of ventilatory control are important causes of repetitive pharyngeal collapse during sleep. Obstructive sleep apnoea can be diagnosed on the basis of characteristic history (snoring, daytime sleepiness) and physical examination (increased neck circumference), but overnight polysomnography is needed to confirm presence of the disorder. Repetitive pharyngeal collapse causes recurrent arousals from sleep, leading to sleepiness and increased risk of motor vehicle and occupational accidents. The surges in hypoxaemia, hypercapnia, and catecholamine associated with this disorder have now been implicated in development of hypertension, but the association between obstructive sleep apnoea and myocardial infarction, stroke, and congestive heart failure is not proven. Continuous positive airway pressure, the treatment of choice for obstructive sleep apnoea, reduces sleepiness and improves hypertension.
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PMID:Obstructive sleep apnoea. 1250 19

Emergency ventilation is an essential component of basic life support. Respiratory emergencies occur far more frequently than cardiac arrest and, if not treated promptly and effectively, may lead to cardiac arrest. Many respiratory emergencies require assisted ventilation to prevent the occurrence of hypoxemia, hypercarbia, and cardiac decompensation. Emergency assisted ventilation is often difficult to perform and is associated with several adverse complications, such as gastric inflation, regurgitation, and pulmonary aspiration. The American Heart Association sponsored conferences in 1999 and 2000 to review and revise guidelines for cardiopulmonary resuscitation. This article reviews the science behind guideline changes related to pulmonary resuscitation and discusses recent advances in emergency airway management, focusing on noninvasive techniques for ventilation (mouth-to-mouth ventilation, bag-mask ventilation) and alternative airway devices (laryngeal mask airway, the Combitube).
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PMID:Advances in airway management. 1247 83

Central sleep apnea syndrome (CSAS) is a disorder characterized by repeated apneic events during sleep with no associated ventilatory effort. CSAS is classified as either hypercapnic or non-hypercapnic. In the hypercapnic form of CSAS, increases in PaCO(2) generally result from reductions in ventilation or outright apneas due to an underlying depression of respiratory drive. Hypercapnic CSAS is common in central hypoventilation syndromes which may be primary (idiopathic) or secondary to other disorders that cause damage to the respiratory center. Non-hypercapnic CSAS is not associated with either a primary reduction in respiratory drive or respiratory muscle weakness. Non-hypercapnic CSAS can be a primary disorder or can occur secondary to high altitude, other medical illnesses such as congestive heart failure and central nervous system disease.
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PMID:[Central sleep apnea syndrome]. 1514 16

Hypertrophic osteoarthropathy (HOA) is a condition that accompanies many seemingly unrelated diseases. It is commonly associated with various clinical conditions such as pregnancy, aging, pulmonary diseases, cancers, and other systemic illnesses. The condition has been attributed to various causes such as platelet abnormalities, hormonal disturbances, and cytokine dysfunction, but the exact underlying mechanism has been elusive. We propose a unifying hypothesis that activation of the adrenergic system is the common thread that links all of the disparate clinical associations of hypertrophic osteoarthropathy. In diseased states, autonomic stimulation may occur as a result of chemoreceptor activation in response to acidosis, hypoxia, or hypercapnia. Examples include sleep apnea, congestive heart failure, renal failure, and tumor-induced hypoxia. In this setting, clinical signs of HOA may be a marker of underlying autonomic dysfunction. Autonomic stimulation may also occur as a normal part of pregnancy or as an abnormal component of aging. The exact pathway linking adrenergic excess to HOA remains to be clarified, but a plausible scenario based on current molecular evidence is offered.
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PMID:Hypertrophic osteoarthropathy may be a marker of underlying sympathetic bias. 1523 3

Cardiovascular and cerebrovascular diseases are the most common diseases in industrialized societies. The main objectives of this article were to summarize the physiological effects of sleep apnea on the circulatory system and to review how treatment of this condition influences cardiovascular disease. Acute sleep apnea has a number of hemodynamic consequences, such as pulmonary and systemic hypertension, increased ventricular afterload and reduced cardiac output, all of which result from sympathetic stimulation, arousal, alterations in intrathoracic pressure, hypoxia and hypercapnia. When chronic, sleep apnea-hypopnea syndrome is associated with systemic hypertension, ischemic heart disease, congestive heart failure, and Cheyne-Stokes respiration in patients with congestive heart failure. Nocturnal treatment with continuous positive airway pressure decreases both the number of central apneic episodes and blood pressure in patients with sleep apnea-hypopnea syndrome and arterial hypertension.
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PMID:[Sleep apnea-hypopnea syndrome and the heart]. 1693 14

Pulmonary hypertension was diagnosed in a former conjoined twin presenting with a ventricular septal defect, moderate congestive heart failure, and dyspnea with hypercapnia due to instable bony chest. He underwent successful corrective cardiac surgery and chest wall reconstruction at the age of 12 months. Subsequently, mechanical ventilation was performed for three months to prevent right heart failure and pulmonary hypertension until thoracic stability allowed the tracheostoma to be closed.
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PMID:Successful cardiac surgery in a former conjoined twin with heart malformation and pulmonary hypertension: an unusual complication of a coronary artery bypass surgery. 1780 85

Cerebral blood flow (CBF) and its distribution are highly sensitive to changes in the partial pressure of arterial CO(2) (Pa(CO(2))). This physiological response, termed cerebrovascular CO(2) reactivity, is a vital homeostatic function that helps regulate and maintain central pH and, therefore, affects the respiratory central chemoreceptor stimulus. CBF increases with hypercapnia to wash out CO(2) from brain tissue, thereby attenuating the rise in central Pco(2), whereas hypocapnia causes cerebral vasoconstriction, which reduces CBF and attenuates the fall of brain tissue Pco(2). Cerebrovascular reactivity and ventilatory response to Pa(CO(2)) are therefore tightly linked, so that the regulation of CBF has an important role in stabilizing breathing during fluctuating levels of chemical stimuli. Indeed, recent reports indicate that cerebrovascular responsiveness to CO(2), primarily via its effects at the level of the central chemoreceptors, is an important determinant of eupneic and hypercapnic ventilatory responsiveness in otherwise healthy humans during wakefulness, sleep, and exercise and at high altitude. In particular, reductions in cerebrovascular responsiveness to CO(2) that provoke an increase in the gain of the chemoreflex control of breathing may underpin breathing instability during central sleep apnea in patients with congestive heart failure and on ascent to high altitude. In this review, we summarize the major factors that regulate CBF to emphasize the integrated mechanisms, in addition to Pa(CO(2)), that control CBF. We discuss in detail the assessment and interpretation of cerebrovascular reactivity to CO(2). Next, we provide a detailed update on the integration of the role of cerebrovascular CO(2) reactivity and CBF in regulation of chemoreflex control of breathing in health and disease. Finally, we describe the use of a newly developed steady-state modeling approach to examine the effects of changes in CBF on the chemoreflex control of breathing and suggest avenues for future research.
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PMID:Integration of cerebrovascular CO2 reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation. 1921 19


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