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

The health risks of obesity increase with its severity and reach significance at a weight greater than 20% above optimal, by using life insurance tables, or at a body mass index greater than 27. Risks include hypertension, insulin resistance and diabetes mellitus, cardiovascular disease, hypertriglyceridemia, low high-density-lipoprotein cholesterol, and, in some studies, high total-and low-density-lipoprotein cholesterol. There is an increased mortality from endometrial cancer in women and from colorectal cancer in men. Chronic hypoxia and hypercapnia, sleep apnea, gout, and degenerative joint disease can occur with more severe obesity. The distribution of body fat is directly related to these health risks. Abdominal obesity is more dangerous than gluteal-femoral obesity because the amount of intraabdominal fat seems to determine much of the increased peril; therefore, risks of cardiovascular disease, stroke, hypertension, and diabetes increase with abdominal obesity, even independently of total fat mass.
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PMID:Health implications of obesity. 203 92

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

Sleep apnea (intermittent periods of hypoxia with or without hypercapnia) is associated with systemic hypertension and increased mortality from cardiovascular disease, but the relationship to pulmonary hypertension is uncertain. Previous studies on intermittent hypoxia (IH) in rats that demonstrated pulmonary hypertension utilized relatively long periods of hypoxia. Recent studies that utilized brief periods of hypoxia have conflicting reports of right ventricular (RV) hypertrophy. In addition, many studies have not measured pulmonary hemodynamics to asses the severity of pulmonary hypertension in vivo. Given the increasing availability of genetically engineered mice and the need to establish a rodent model of IH-induced pulmonary hypertension, we studied the effect of IH (2-min cycles of 10% and 21% O2, 8 h/day, 4 wk) on wild-type mice, correlating in vivo measurements of pulmonary hypertension with RV mass and pulmonary vascular remodeling. RV systolic pressure was increased after IH (36 +/- 0.9 mmHg) compared with normoxia (29.5 +/- 0.6) but was lower than continuous hypoxia (44.2 +/- 3.4). RV mass [RV-to-(left ventricle plus septum) ratio] correlated with pressure measurements (IH = 0.27 +/- 0.02, normoxia = 0.22 +/- 0.01, and continuous hypoxia = 0.34 +/- 0.01). Hematocrits were also elevated after IH and continuous hypoxia (56 +/- 1.6 and 54 +/- 1.1 vs. 44.3 +/- 0.5%). Evidence of neomuscularization of the distal pulmonary circulation was found after IH and continuous hypoxia. We conclude that mice develop pulmonary hypertension following IH, representing a possible animal model of pulmonary hypertension in response to the repetitive hypoxia-reoxygenation of sleep apnea.
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PMID:Selected Contribution: Pulmonary hypertension in mice following intermittent hypoxia. 1135 19

The mechanisms underlying the link between obstructive sleep apnoea (OSA) and cardiovascular disease are not completely established. However, there is increasing evidence that autonomic mechanisms are implicated. A number of studies have consistently shown that patients with OSA have high levels of sympathetic nerve traffic. During sleep, repetitive episodes of hypoxia, hypercapnia and obstructive apnoea act through chemoreceptor reflexes and other mechanisms to increase sympathetic drive. Remarkably, the high sympathetic drive is present even during daytime wakefulness when subjects are breathing normally and no evidence of hypoxia or chemoreflex activation is apparent. Several neural and humoral mechanisms may contribute to maintenance of higher sympathetic activity and blood pressure. These mechanisms include chemoreflex and baroreflex dysfunction, altered cardiovascular variability, vasoconstrictor effects of nocturnal endothelin release and endothelial dysfunction. Long-term continuous positive airway pressure treatment decreases muscle sympathetic nerve activity in OSA patients. The vast majority of OSA patients remain undiagnosed. Unrecognized OSA may contribute, in part, to the metabolic and cardiovascular derangements that are thought to be linked to obesity, and to the association between obesity and cardiovascular risk. Furthermore, acting through sympathetic neural mechanisms, OSA may contribute to or augment elevated levels of blood pressure in a large proportion of the hypertensive patient population.
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PMID:Sympathetic nerve activity in obstructive sleep apnoea. 1260 10

Respiratory failure is still an important complication of chronic obstructive pulmonary disease (COPD) and hospitalisation with an acute episode being a poor prognostic marker. However, other comorbid conditions, especially cardiovascular disease, are equally powerful predictors of mortality. The physiological basis of acute respiratory failure in COPD is now clear. Significant ventilation/perfusion mismatching with a relative increase in the physiological dead space leads to hypercapnia and hence acidosis. This is largely the result of a shift to a rapid shallow breathing pattern and a rise in the dead space/tidal volume ratio of each breath. This breathing pattern results from adaptive physiological responses which lessen the risk of respiratory muscle fatigue and minimise breathlessness. Treatment is directed at reducing the mechanical load applied to each breath, correcting specific precipitating factors, e.g. bacterial infection, and maintaining gas exchange. Both bronchodilators and oral corticosteroids can improve spirometric results in exacerbations of COPD and should be routinely offered to patients with respiratory failure. Controlled oxygen is still not always prescribed appropriately and high inspired oxygen concentrations can lead to severe acidosis by either worsening ventilation/perfusion mismatching and/or inducing a degree of hypoventilation. Ventilatory support using noninvasive ventilation has revolutionised the approach to these patients. Acute respiratory failure due to chronic obstructive pulmonary disease remains a common medical emergency that can be effectively managed. More attention should be focused on the prevention of these episodes and identifying the factors which cause early relapse.
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PMID:Respiratory failure in chronic obstructive pulmonary disease. 1462 Nov 14

Rosiglitazone is a peroxisome proliferator active receptor. gamma agonist, which increases insulin sensitivity in adipose tissue, muscle, and liver. Rosiglitazone is a member of the thiazolidinedione group, and because of its significantly positive effect on glycemic control, it is especially preferred in type 2 diabetic patients with a high cardiovascular disease risk. This drug, because of its decreasing effect on insulin resistance, is used alone or combined with type 2 diabetic drugs. A 73-year-old female patient was admitted to the emergency department with dyspnea, pink frothing phlegm, cyanosis, and tiredness. She was lethargic, uncooperative, and had no orientation. In arterial blood gases, hypoxemia and hypercapnia were found. She was taken to the general intensive care unit, and oxygen was applied via mask. The patient had a history of 10 years of diabetes mellitus, hypertension, and atherosclerotic cardiac disease, and she was using rosiglitazone for the past 6 weeks. Her chest x-ray was taken, and acute pulmonary edema was diagnosed. In her last echocardiography, which was performed 1 year before, no signs indicating cardiac failure and pleural effusion could be found. Therefore, it was concluded that pulmonary edema occurred as a complication of rosiglitazone use. After stabilizing the patient's vital signs, blood glucose levels, and lactate levels, medical treatment of diabetes mellitus was rearranged, and she was discharged on the seventh day after her admittance. In a patient with diabetes mellitus who has been admitted to the intensive care unit because of acute pulmonary edema, for differential diagnosis, use of rosiglitazone should be kept in mind during the determination of treatment. Therefore, the authors aim to discuss the effect of rosiglitazone on creating acute pulmonary edema with a case report presentation.
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PMID:Acute pulmonary edema due to rosiglitazone use in a patient with diabetes mellitus. 1669 44

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

Preterm birth and chronic lung disease may increase the risk of hypertension and cardiovascular disease in infancy and adolescence. Here we looked for evidence of early circulatory dysfunction associated with these perinatal complications. We compared infants born at term (n = 12) with those born preterm with an uncomplicated neonatal course (n = 12) or diagnosed with bronchopulmonary dysplasia (BPD) (n = 10). We measured blood pressure (BP) (Finometer), and heart rate (HR) responses to 4 min of breathing 4% CO2 during quiet sleep. Hypercapnia accelerated HR and increased BP of term infants. Preterm infants either (i) had an exaggerated pressor but little or no HR response to CO2 (healthy or mild-moderate BPD) or (ii) had a diminished pressor response and accompanying decrease in HR (severe BPD). Short-term reflex cardiovascular control was consequently altered by premature birth, with potentially more serious aberrations associated with severe BPD. Most anomalies had not resolved by the time infants born preterm reached term age; some may be early signs of emerging long-term cardiovascular dysfunction.
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PMID:Abnormal circulatory stress responses of preterm graduates. 1731 92

Sleep apnea has been linked to excessive daytime sleepiness, depressed mood, hypertension, and cardiovascular disease in the general population. The prevalence of severe sleep apnea in the conventional thrice-weekly hemodialysis population has been estimated to be more than 50%. Sleep apnea leads to repetitive episodes of hypoxemia, hypercapnia, sleep disruption, and activation of the sympathetic nervous system. The hypoxemia, arousals, and intrathoracic pressure changes associated with sleep apnea lead to sympathetic activation, endothelial dysfunction, oxidative stress, and inflammation. Because sleep apnea has been shown to be widespread in the conventional dialysis population, it may be that sleep apnea contributes substantially to the sleepiness, poor quality of life, and cardiovascular disease found in this population. The causal links between conventional dialysis and sleep apnea remain speculative, but there are likely multiple factors related to volume status and azotemia that contribute to the high rate of severe sleep apnea in dialysis patients. Both nocturnal automated peritoneal dialysis and nocturnal hemodialysis have been associated with reduced severity of sleep apnea. Nocturnal dialysis modalities may provide tools to increase our understanding of the uremic sleep apnea and may also provide therapeutic alternatives for end-stage renal disease patients with severe sleep apnea. In conclusion, sleep apnea is an important, but overlooked, public health problem for the dialysis population. The impact of sleep apnea treatment in this high-risk population may include reduced sleepiness, better mood and blood pressure, and lowered risk of cardiovascular disease.
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PMID:Sleep apnea and dialysis therapies: things that go bump in the night? 1792 30

Obesity hypoventilation syndrome (OHS) is characterized by obesity, daytime hypercapnia, and sleep-disordered breathing in the absence of significant lung or respiratory muscle disease. Compared with eucapnic morbidly obese patients and eucapnic patients with sleep-disordered breathing, patients with OHS have increased health care expenses and are at higher risk of developing serious cardiovascular disease leading to early mortality. Despite the significant morbidity and mortality associated with this syndrome, diagnosis and institution of effective treatment occur late in the course of the syndrome. Given that the prevalence of extreme obesity has increased considerably, it is likely that clinicians will encounter patients with OHS in their clinical practice. Therefore maintaining a high index of suspicion can lead to early recognition and treatment reducing the high burden of morbidity and mortality and related health care expenditure associated with undiagnosed and untreated OHS. In this review we define the clinical characteristics of the syndrome and review the pathophysiology, morbidity, and mortality associated with it. Last, we discuss currently available treatment modalities.
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PMID:Assessment and management of patients with obesity hypoventilation syndrome. 1825 Feb 15


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