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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cardiorespiratory responses were examined in yellowtail, Seriola quinqueradiata exposed to two levels of hypercapnia (seawater equilibrated with a gas mixture containing 1% CO(2) (water PCO(2) = 7 mmHg) or 5% CO(2) (38 mmHg)) for 72 hr at 20 degrees C. Mortality was 100% within 8 hr at 5% CO(2), while no fish died at 1% CO(2). No cardiovascular variables (cardiac output, Q; heart rate, HR; stroke volume, SV and arterial blood pressure, BP) significantly changed from pre-exposure values during exposure to 1% CO(2). Arterial CO(2) partial pressure (PaCO(2)) significantly increased (P < 0.05), reaching a new steady-state level after 3 hr. Arterial blood pH (pHa) decreased initially (P < 0.05), but was subsequently restored by elevation of plasma bicarbonate ([HCO(3)(-)]). Arterial O(2) partial pressure (PaO(2)), oxygen content (CaO(2)), and hematocrit (Hct) were maintained throughout the exposure period. In contrast, exposure to 5% CO(2) dramatically reduced Q (P < 0.05) through decreasing SV (P < 0.05), although HR did not change. BP was transiently elevated (P < 0.05), followed by a precipitous fall before death. The pHa was restored incompletely despite a significant increase in [HCO(3)(-)]. PaO(2) decreased only shortly before death, whereas CaO(2) kept elevated due to a large increase in Hct (P < 0.05). We tentatively conclude that cardiac failure is a primary physiological disorder that would lead to death of fish subjected to high environmental CO(2) pressures.
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PMID:Effects of lethal levels of environmental hypercapnia on cardiovascular and blood-gas status in yellowtail, Seriola quinqueradiata. 1271 43

Heart failure is a highly prevalent problem associated with excess morbidity and mortality and economic impact. Because of increased average life span, improved therapy of ischemic coronary artery disease and hypertension, the incidence and prevalence of heart failure will continue to rise into the twenty-first century. Multiple factors may contribute to the progressively declining course of heart failure. One such cause could be the occurrence of repetitive episodes of apnea, hypopnea, and hyperpnea, which frequently occur in patients with heart failure. Episodes of apnea, hypopnea, and hyperpnea cause sleep disruption, arousals, intermittent hypoxemia, hypercapnia, hypocapnia, and changes in intrathoracic pressure. These pathophysiologic consequences of sleep-related breathing disorders have deleterious effects on cardiovascular system, and the effects may be most pronounced in the setting of established heart failure and coronary artery disease. Diagnosis and treatment of sleep-related breathing disorders may improve morbidity and mortality of patients with heart failure [34]. Large-scale, carefully executed therapeutic studies are needed to determine if treatment of sleep-related breathing disorders changes the natural history of left ventricular failure.
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PMID:Heart failure and sleep apnea: emphasis on practical therapeutic options. 1280 Jul 79

Chronic obstructive pulmonary disease (COPD) often leads to massive oedema and the development of what is usually called cor pulmonale. The mechanisms by which patients with COPD retain salt and water are not completely understood. Several abnormalities have been found including reduced renal blood flow with relatively preserved glomerular filtration rate and elevated levels of renin, aldosterone, arginine vasopressin and atrial natriuretic peptide. Generally, these abnormalities worsen with the severity of COPD and are most marked during the oedematous phases. Cardiac output is remarkably normal, suggesting that "cor pulmonale" is not primarily a cardiac disorder but rather a condition of volume overload due to activation of sodium-retaining mechanisms. The stimulus for this activation could be underfilling of the arterial system (reduced effective circulating volume) secondary to a fall in total peripheral vascular resistance. The latter is caused by hypercapnia-induced dilation of the precapillary sphincters. Apparently, the massive sodium retention by the kidney is not able to restore the circulating volume and a vicious cycle ensues ultimately leading to a clinical picture which resembles right-sided heart failure. Predictably, only blockade of the effects of carbon dioxide at the level of the precapillary sphincters would be able to halt this process.
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PMID:Fluid homeostasis in chronic obstructive lung disease. 1462 Nov 5

This case report discusses the cause of death in a 3-year-old child who survived a high dose (20 mg x kg-1 x h-1) of propofol, infused over a period of 15 h, following which the patient developed a combined respiratory and metabolic acidosis, the oxygenation remaining normal. Bronchospasm was assumed to be the cause of hypercapnia. At this time the doctors in charge did not think of a possible side-effect of propofol. The administration of propofol was interrupted, the patient recovered within 13 h from the acidosis, woke up and required further sedation. A supposedly entirely safe infusion of 4 mg x kg-1 x h-1 propofol, as recommended in the literature for up to 48 h, was administered. After only 8 h intractable bradycardic dysrhythmias occurred. Although pharmacokinetic studies have pointed to a possible accumulation of propofol during continuous infusions, an interruption of an infusion for several hours has been considered sufficient for practically total clearance of the drug from the body. In this case re-exposure with a recommended dose of propofol was accompanied by bradycardia and dysrythmias that proved to be resistant to therapy and led to fatal cardiac insufficiency with a functioning artificial pacemaker in place. This case raises concerns about the safety of long-term infusions of propofol for sedation in children and possibly also in adults.
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PMID:Death after re-exposure to propofol in a 3-year-old child: a case report. 1499 68

Sudden infant death syndrome is the leading cause of death in infancy, but its pathophysiological mechanism has been elusive. Sudden death in adults is a common phenomenon, but the etiology in many cases remains unknown at autopsy. We hypothesize that maladaptive sympathetic bias is the explanatory mechanism that links many cases of sudden demise among adults and infants as companion syndromes. Normally, sympathetic response occurs as an adaptation to physiologic demands of the body through various autonomic reflex arcs such as chemoreceptors. Sympathetic response can become chronic and maladaptive when the normal sympathetic response fails to correct the precipitating physiologic trigger, leading to chronic activation of autonomic reflex arcs. In conditions such as infant sleep apnea or adult heart failure, a pernicious cycle of sympathetic bias may result. Chronic sympathetic bias increases susceptibility to sudden fatal arrhythmias, QT-related and otherwise, in the setting of an exaggerated adrenergic challenge. Examples of such adrenergic stressors include trauma, hypoxia, hypercapnia, acidosis, sleep arousal, illness, medical procedures, and physical activity, all of which have associations with sudden death. Our hypothesis may not only help explain the survival benefits of drugs such as beta-blockers and devices such as synchronization therapy, but also portend new application of similar therapies for many conditions of sympathetic bias.
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PMID:Sudden death among infants and adults: companion disorders of maladaptive sympathetic bias. 1514 36

Heart failure is a highly prevalent disorder, with significant economic impact, and is associated with excess morbidity and mortality. One factor that may contribute to the progressively declining course of heart failure is the occurrence of recurrent episodes of apnea and hypopnea. There are two major kinds of sleep-related breathing disorders: obstructive and central sleep apnea. In patients with heart failure, in contrast to the general population, central sleep apnea is the most common form of sleep-related breathing disorder. Episodes of apnea, hypopnea, and the subsequent hyperpnea cause sleep disruption, arousals, hypoxemia-reoxygenation, hypercapnia/hypocapnia, and changes in intrathoracic pressure. These pathophysiologic consequences of sleep-related breathing disorders have deleterious effects on the cardiovascular system, and may be even more pronounced in the setting of established heart failure and coronary artery disease. Therefore, sleep apnea in heart failure should be treated. Central sleep apnea may be treated with nocturnal supplemental nasal oxygen, theophylline, or nasal-positive pressure devices, such as nasal continuous positive airway pressure (CPAP). The treatment of choice for obstructive sleep apnea is nasal CPAP. Although long-term controlled trials of the effect of treatment of sleep apnea on mortality in patients with heart failure are still pending, treatment of sleep apnea, both obstructive and central, does result in a decrease in sympathetic activity and an improvement in systolic function, which are known surrogates of mortality. Therefore, diagnosis and treatment of sleep-related breathing disorders may increase survival of patients with heart failure.
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PMID:Prevalence and treatment of breathing disorders during sleep in patients with heart failure. 1600 60

In obstructive sleep apnea syndrome (OSAS), repetitive episodes of apnea cause increased sympathetic nerve activity, increased surges in arterial blood pressure, swings in intrathoracic pressure, oxidative stres, hypoxia and hypercapnia. The association of OSAS with some diseases, having endothelial dysfunction in their physiopathology, such as hypertension, diabetes mellitus, obesity, coronary artery diseases, stroke and heart failure is common. Increased sympathetic nerve activity and also endothelial dysfunction which are the results of hypoxia, have important roles in vascular complications of OSAS. When compared with healthy population, an important endothelial dysfunction in OSAS patients and relationship between OSAS severity and endothelial dysfunction have been shown. In this review, the relationship between OSAS and endothelial dysfunction was overviewed.
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PMID:[Obstructive sleep apnea syndrome, endothelial dysfunction and coronary atherosclerosis]. 1625 93

Sympathetic activation and sleep apnea are present in most patients with symptomatic systolic heart failure (HF). Acutely, obstructive and central apneas increase muscle sympathetic activity (MSNA) during sleep by eliciting recurrent hypoxia, hypercapnia, and arousal. In obstructive sleep apnea patients with normal systolic function, this increase persists after waking. Whether coexisting sleep apnea augments daytime MSNA in HF is unknown. We tested the hypothesis that its presence exerts additive effects on MSNA during wakefulness. Overnight sleep studies and morning MSNA recordings were performed on 60 subjects with ejection fraction <45%. Of these, 43 had an apnea-hypopnea index > or =15 per hour. Subjects with and subjects without sleep apnea were similar for age, ejection fraction, HF etiology, body mass index, blood pressure, and heart rate. Daytime MSNA was significantly higher in those with sleep apnea (76+/-2 versus 63+/-4 bursts per 100 heartbeats [mean+/-SEM], P=0.005; 58+/-2 versus 50+/-3 bursts/min, P=0.037), irrespective of its etiology (the mean difference for central sleep apnea was 17 bursts per 100 heartbeats; n=14; P=0.006; and for obstructive sleep apnea, 11 bursts per 100 heartbeats; n=29; P=0.032). In a subgroup (n=8), treatment of obstructive sleep apnea lowered MSNA by 12 bursts per 100 heartbeats (P=0.003). Convergence of independent excitatory influences of HF and sleep apnea on central sympathetic neurons results in higher MSNA during wakefulness in HF patients with coexisting sleep apnea. This additional stimulus to central sympathetic outflow may accelerate the progression of HF; its attenuation by treatment of sleep apnea represents a novel nonpharmacological opportunity.
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PMID:Muscle sympathetic nerve activity during wakefulness in heart failure patients with and without sleep apnea. 1628 69

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

Respiratory failure as a result of overload and/or reduced capacity of the respiratory muscles is the most common cause of unsuccessful weaning and the need for long term mechanical ventilation. Chronic obstructive pulmonary disease (COPD) is the most common underlying cause leading into long term mechanical ventilation. The most important clinical parameter for fatigue of the respiratory muscles is the rapid shallow breathing index. Other essential factors which impact weaning failure, are the underlying diseases (e. g. neuromuscular disease or heart failure), micro- and macro aspiration, malnutrition, anemia and obesity. A protocol based strategy to discontinue mechanical ventilation and the use of weaning predictors are helpful. Nonetheless the experienced physician is irreplacable in the weaning process. Reconditioning of the respiratory muscles is the main focus during weaning after long term mechanical ventilation and all therapeutic measures should be targeted to unload the fatiguing respiratory muscles. With the widely used assisted ventilation modes, the inspiratory work of breathing is still significantly increased. Only controlled mechanical ventilation (pressure- or volume controlled), which may also be applied to unsedated patients when individually adapted, offers the best possible relief and recovery of the respiratory muscles. Additional strategies, such as the balancing of anemia, reduction of the respiratory drive with i. e. morphine derivates, oxygen therapy during spontaneous-breathing trials and supine position for patients with obesity contribute to the recovery. Particularly patients with chronic lung diseases with hypercapnia benefit from the use of non invasive ventilation (NIV) after extubation to prevent postextubation failure and even after tracheostomy. However, NIV should only be applied under close monitoring and in cooperative patients, always considering the limits of the method. Dying under mechanical ventilation in the end stage illness is still a challenge for all involved persons. In the end stage of their disease for some patients it is possible to discontinue mechanical ventilation so they can spend the last period of their lives on a normal ward or even at home.
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PMID:[Difficult weaning]. 1704 78


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