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Effect of Ventilation Therapy on Mortality Rate Among Obesity Hypoventilation Syndrome and Obstructive Sleep Apnoea Patients

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Introduction: The prevalence of obesity is continually increasing worldwide, which increases the incidence of obesity hypoventilation syndrome (OHS) and its consequent mortality. Methods: We reviewed the therapy mode, comorbidity

The effects of localized hypoventilation on ventilation/perfusion (V/Q) ratios and gas exchange in the dog lung.

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1. Hypoventilation of one lobe of lung was studied in open-chest anaesthetized dogs. Lobar blood flow, pulmonary-artery pressure and gas exchange were measured, the latter from breath-by-breath analysis with a mass spectrometer. 2. Hypoventilation of the lobe by reducing the respiratory pump stroke

Effects of hypoventilation on the cardiovascular responses of rats to adrenaline and acetylcholine.

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Blood pressure and pulse rate in response to administered adrenaline and acetylcholine during hypoventilation were studied in urethane-anaesthetized rats. Hypoventilation was induced by decreasing the stroke volume of artificial ventilation from 1 ml/100 g to 0.3 ml/100 g. There was a significant

Risk of Left Atrial Enlargement in Obese Patients With Obesity-Induced Hypoventilation Syndrome vs Obstructive Sleep Apnea.

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UNASSIGNED Obstructive sleep apnea (OSA) is a known risk factor for atrial fibrillation (AF) that is principally driven by left atrial enlargement. The impact of hypoventilation caused by obesity-induced hypoventilation syndrome (OHS) on left atrial diameter has not been examined. We investigated

Effectiveness of prostaglandin E1 on pulmonary hypertension and right cardiac function induced by single-lung ventilation and hypoventilation.

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It is known that prostaglandin E1 (PGE1) is a potent vasodilator and improves red cell deformability. Single lung-ventilation sometimes occurs under lung transplantation, lung cancer surgery and traumatic pneumonectomy, and may result in increased pulmonary resistance, right heart failure and severe

Cardiovascular responses during hypoventilation at exercise.

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This study aimed to determine the cardiovascular responses during a prolonged exercise with voluntary hypoventilation (VH). 7 men performed 3 series of 5-min exercise at 65% of normoxic maximal O (2) uptake under 3 conditions: (1) normal breathing (NB) in normoxia (NB (0.21)), (2) VH in normoxia (VH

Stroke Anticoagulation

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Stroke is one of the leading causes of death and long-term disability worldwide.[1][2] As medical management advances, the incidence and mortality rate of stroke declines, with the majority of strokes presenting as ischemic strokes vs. hemorrhagic strokes. As such, the focus of this article will be

Central Hypoventilation: A Rare Complication of Wallenberg Syndrome.

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Central alveolar hypoventilation disorders denote conditions resulting from underlying neurologic disorders affecting the sensors, the central controller, or the integration of those signals leading to insufficient ventilation and reduction in partial pressures of oxygen. We report a patient who

Hypoxic ventilatory depression in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes.

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We describe a case of a 21-year-old man with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) who presented with hypoxic ventilatory depression. He had chronic hypoventilation, which was not explained by weakness of respiratory muscles. His hypercapnic

Central alveolar hypoventilation (Ondine's curse) caused by megadolichobasilar artery.

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Central alveolar hypoventilation (CAH) syndrome is a clinical condition that is characterized by the loss of automatic breathing, particularly during sleep. Most forms in adults are caused by brainstem ischemia, mass, infection, demyelinating disease, or anoxic-ischemic damage. We present a case of

Passive motion of the extremities modifies alveolar ventilation during sleep in patients with congenital central hypoventilation syndrome.

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Passive motion of lower extremities (PMLE) elicits significant increases in alveolar ventilation (V A) in awake children with congenital central hypoventilation syndrome (CCHS), who have absent or near absent ventilatory responses to hypercapnia. We hypothesized that PMLE would improve V A during

Cardiovascular disorders and obstructive sleep apnea syndrome.

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The first polysomnographic recordings with concomitant monitoring of cardiocirculatory parameters demonstrated that obstructive apneas arising during sleep are accompanied by a marked increase in pulmonary and systemic arterial pressure and severe alveolar hypoventilation. Apneas also may give rise

Comparison of the cardiorespiratory effects of a combination of ketamine and propofol, propofol alone, or a combination of ketamine and diazepam before and after induction of anesthesia in dogs sedated with acepromazine and oxymorphone.

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OBJECTIVE To evaluate the cardiorespiratory effects of IV administration of propofol (4 mg/kg), ketamine hydrochloride and propofol (2 mg/kg each; K-P), or ketamine hydrochloride (5 mg/kg) and diazepam (0.2 mg/kg; K-D) before and after induction of anesthesia (IoA) in dogs sedated with acepromazine

Effects of desflurane and mode of ventilation on cardiovascular and respiratory functions and clinicopathologic variables in horses.

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OBJECTIVE To quantitate the effects of desflurane and mode of ventilation on cardiovascular and respiratory functions and identify changes in selected clinicopathologic variables and serum fluoride values associated with desflurane anesthesia in horses. METHODS 6 healthy adult horses. METHODS Horses

Influence of a constant rate infusion of dexmedetomidine on cardiopulmonary function and recovery quality in isoflurane anaesthetized horses.

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OBJECTIVE To investigate the influence of a dexmedetomidine constant rate infusion (CRI) in horses anaesthetized with isoflurane. METHODS Prospective, randomized, blinded, clinical study. METHODS Forty adult healthy horses (weight mean 491 ± SD 102 kg) undergoing elective surgery. METHODS After

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