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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After uneventful ENT surgery, two male patients developed acute upper airway obstruction following extubation which progressed into negative pressure pulmonary edema (NPPE). One of these two patients suffered from known obstructive sleep apnoea syndrome, the other admitted to heavy snoring only after the incident. The pathophysiology of NPPE and the anaesthesiological implications of a patient's history of snoring are discussed.
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PMID:[Snoring and postoperative pulmonary edema]. 1076 54

We investigated the frequency of undiagnosed sleep apnea in patients scheduled for elective total joint arthroplasty. Two hundred fifty-four patients were assessed between September 1999 and May 2001. At intake, patients were given a standard systems review with the addition of targeted questions about sleep apnea. Ten patients reported symptoms consistent with undiagnosed obstructive sleep apnea (OSA). The identification of undiagnosed OSA is an issue for orthopedic practice because many patients referred to an arthroplasty service for hip and/or knee surgeries are obese. A few screening questions, readily incorporated into the preoperative assessment, may prevent perioperative complications such as postextubation airway obstruction, negative pressure pulmonary edema, or opioid-induced airway obstruction.
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PMID:Incidence of undiagnosed sleep apnea in patients scheduled for elective total joint arthroplasty. 1465 10

Humans encounter hypoxia throughout their lives. This occurs by destiny in utero, through disease, and by desire, in our quest for altitude. Hypoxic pulmonary vasoconstriction (HPV) is a widely conserved, homeostatic, vasomotor response of resistance pulmonary arteries to alveolar hypoxia. HPV mediates ventilation-perfusion matching and, by reducing shunt fraction, optimizes systemic Po(2). HPV is intrinsic to the lung, and, although modulated by the endothelium, the core mechanism is in the smooth muscle cell (SMC). The Redox Theory for the mechanism of HPV proposes the coordinated action of a redox sensor (the proximal mitochondrial electron transport chain) that generates a diffusible mediator [a reactive O(2) species (ROS)] that regulates an effector protein [voltage-gated potassium (K(v)) and calcium channels]. A similar mechanism for regulating O(2) uptake/distribution is partially recapitulated in simpler organisms and in the other specialized mammalian O(2)-sensitive tissues, including the carotid body and ductus arteriosus. Inhibition of O(2)-sensitive K(v) channels, particularly K(v)1.5 and K(v)2.1, depolarizes pulmonary artery SMCs, activating voltage-gated Ca(2+) channels and causing Ca(2+) influx and vasoconstriction. Downstream of this pathway, there is important regulation of the contractile apparatus' sensitivity to calcium by rho kinase. Controversy remains as to whether hypoxia decreases or increases ROS and which electron transport chain complex generates the ROS (I and/or III). Possible roles for cyclic adenosine diphosphate ribose and an unidentified endothelial constricting factor are also proposed by some groups. Modulation of HPV has therapeutic relevance to cor pulmonale, high-altitude pulmonary edema, and sleep apnea. HPV is clinically exploited in single-lung anesthesia, and its mechanisms intersect with those of pulmonary arterial hypertension.
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PMID:Hypoxic pulmonary vasoconstriction. 1559 9

Lung and kidney function are intimately related in both health and disease. Respiratory changes help to mitigate the systemic effects of renal acid-base disturbances, and the reverse is also true, although renal compensation occurs more slowly than its respiratory counterpart. A large number of diseases affect both the lungs and the kidneys, presenting most often with alveolar hemorrhage and glomerulonephritis. Most of these conditions are uncommon or rare, although three of them--Wegener's granulomatosis, systemic lupus erythematosus, and Goodpasture's syndrome--are not infrequently encountered by respiratory care clinicians. Respiratory complications of chronic renal failure include pulmonary edema, fibrinous pleuritis, pulmonary calcification, and a predisposition to tuberculosis. Urinothorax is a rare entity associated with obstructive uropathy. Sleep disturbances are extremely common in patients with end-stage renal disease, with sleep apnea occurring in 60% or more of such patients. The management of patients with acute renal failure is frequently complicated by pulmonary edema and the effects of both fluid overload and metabolic acidosis. These processes affect the management of mechanical ventilation in such patients and may interfere with weaning. Successful lung-protective ventilation in patients with acute lung injury and renal failure may require modification of hemodialysis in order to combat severe acidemia. Hemodialysis-related hypoxemia, which was once believed to be the result of pulmonary leukostasis and complement activation, is explained by diffusion of CO2 into the dialysate, with concomitant alveolar hypoventilation in the process of maintaining a normal P(aCO2). Like acute lung injury, renal failure is a common complication of critical illness. An increasing body of evidence also supports the notion that the kidneys, like the lungs, are susceptible to injury induced as a result of positive-pressure mechanical ventilation.
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PMID:Respiratory considerations in the patient with renal failure. 1656 95

The case of a morbidly obese 3.5-year-old boy, with Prader-Willi syndrome (PWS), who experienced a life-threatening episode of pulmonary edema soon after induction of general anesthesia with sevoflurane and intubation for orchidopexy is presented. The patient who had history of sleep apnea and who had an uneventful laparoscopy under general anesthesia 6 months previously was supported with mechanical ventilation with positive end expiratory pressure but developed hyperthermia, pneumonia, sepsis, and Acute Respiratory Distress Syndrome in the intensive care unit. He recovered fully 11 days after surgery. The possible contributing factors for the development of pulmonary edema are discussed. Arrangements for monitoring in an intensive care setting after surgery are highly recommended for patients with PWS.
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PMID:Near demise of a child with Prader-Willi syndrome during elective orchidopexy. 1687 24

We observed improvements in two cases of chronic atelectasis through use of nasal continuous positive airway pressure (nCPAP). Case 1 suffered from middle lobe syndrome accompanied by chronic atelectasis resistant to medical treatment. Case 2 suffered from respiratory failure caused by chronic atelectasis and airway infection complications thereof following a total pneumonectomy and post-pneumonectomy syndrome. The patient was placed on artificial ventilation, and atelectasis was improved by maintaining PEEP and airflow to the atelectatic region. Following extubation we obtained good pneumatization using nCPAP. nCPAP has been reported as effective not only in cases of sleep apnea, but also for cardiogenic pulmonary edema and post-operative atelectasis; we believe it holds great promise for chronic atelectasis as well.
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PMID:[Two cases of chronic atelectasis that improved through use of nasal continuous positive pressure]. 1764 49

A patent foramen ovale (PFO) is a common finding present in 25% of the population. A relationship between PFO and several clinical conditions such as stroke, migraine, platypnea-orthodeoxia syndrome, neurological decompression illness in divers, high altitude pulmonary edema, sleep apnea, and economy class syndrome have been documented. Observational non-randomized studies have shown percutaneous PFO closure more effective than medical treatment for stroke prevention, in particular in patients with complete closure as well as in patients with more than one cerebrovascular event at baseline. In the case of migraine, PFO closure has been shown to result in a marked reduction in migraine burden or migraine days. PFO anatomy, epidemiological data on associated clinical conditions, comparison between percutaneous closure and medical treatment, as well as the technical aspect of the procedure are described in this review.
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PMID:Percutaneous closure of the patent foramen ovale. 1791 71

In this report we describe a patient with recurrent episodes of acute pulmonary oedema after aortic and mitral valve surgery. The first episode of pulmonary oedema was caused by mitral valve dysfunction. The second episode of pulmonary oedema was not clearly associated with a mitral valve problem, but reoperation was performed in the absence of another explanation. After the third episode of acute pulmonary oedema occurred, the diagnosis of obstructive sleep apnoea syndrome (OSAS) was considered and confirmed. After starting treatment with continuous positive airway pressure (CPAP) during his sleep the patient had no further episodes of acute respiratory failure. Our case demonstrates that acute pulmonary oedema after cardiothoracic surgery can be caused or at least be precipitated by OSAS and should be suspected in patients with unexplained episodes of (recurrent) pulmonary oedema. (Neth Heart J 2008;16:310-2.).
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PMID:Recurrent acute pulmonary oedema after aortic and mitral valve surgery due to trachea malacia and obstructive sleep apnoea syndrome. 1882 75

Sleep plays a large role in patients with heart failure. In normal subjects, sleep is usually in a supine position with reduced sympathetic drive, elevated vagal tone and as such a relatively lower cardiac output and minute ventilation, allowing for recuperation. Patients with heart failure may not experience the same degree of autonomic activity change and the supine position may place a large strain on the pulmonary system. More than half of all heart failure patients have one of two types of sleep apnea: either obstructive or central sleep apnea. Some patients have both types. Obstructive sleep apnea is likely to be a cause of heart failure due to large negative intrathoracic pressures, apnea related hypoxemia and hypercapnia, terminated by an arousal and surge in systemic blood pressure associated with endothelial damage and resultant premature atherosclerosis. Reversal of obstructive sleep apnea improves blood pressure, systolic contraction and autonomic dysfunction however mortality studies are lacking. Central sleep apnea with Cheyne Stokes pattern of respiration (CSA-CSR) occurs as a result of increased central controller (brainstem driving ventilation) and plant (ventilation driving CO2) gain in the setting of a delayed feed back (i.e., low cardiac output). It is thought this type of apnea is a result of moderately to severely impaired cardiac function and is possibly indicative of high mortality. Treatment of CSA-CSR is best undertaken by treating the underlying cardiac condition which may include with medications, pacemakers, transplantation or continuous positive airway pressure (CPAP). In such patients CPAP exerts unique effects to assist cardiac function and reduce pulmonary edema. Whether CPAP improves survival in this heart failure population remains to be determined.
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PMID:Sleep in heart failure. 1911 Jan 35

High altitude changes human physiology and can result in illnesses such as acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema. The physiological impacts of high-altitude illnesses occur secondary to extravasation of fluid from the intravascular space into the extravascular space during a rapid ascent. Headache, hearing disturbances, vestibular disturbances, epistaxis, sleep apnea, coughing, respiratory tract infections, and nasal obstruction are main ear, nose, and throat complaints of individuals travelling to high altitude. These complaints can cause delays or cancelations in a person's climbing plans. In this article, we review the ear, nose, and throat effects of high altitude based on the relevant literature.
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PMID:Ear, nose, and throat effects of high altitude. 1955 97


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