Sleep
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Recent studies show that central sleep apnea occur in about 40% of patients with heart failure and systolic dysfunction. The pathophysiological consequences of central sleep apnea may contribute to morbidity and mortality of heart failure. Three treatment modalities, oxygen, continuous positive airway pressure and theophylline have been shown to decrease periodic breathing modestly with considerable improvement in arterial oxyhemoglobin desaturation, and variable effects on sleep characteristics. However, long-term effects of central sleep apnea and its treatment on the natural history of heart failure remain to be determined.
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Decrease of respiratory muscle capacities in neuromuscular disease can lead to chronic respiratory failure with permanent alveolar hypoventilation. Respiratory centers elaborate a strategy of breathing dedicated to prevent overt respiratory muscles fatigue. This strategy may worsen chronic hypercapnia. ⋯ The effects of atonia are amplified by a very low reactivity of respiratory centers. Nocturnal mechanical ventilation improves nocturnal hypoventilation and daytime arterial blood gases (ABG). Mechanism of improvement in ABG and how nocturnal hypoventilation and diurnal hypoventilation interact, are still a matter of debate.
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Obstructive sleep apnea (OSA) has been identified and recorded in paediatric patients, the potential mechanisms for OSA include anatomical abnormalities that lead to a narrowed airway space, reduced muscle tone and abnormal central ventilatory control. Several treatments have been developed and are routinely used to treat OSA in infants and children. ⋯ Surgery to correct underlying anatomical abnormalities is frequently used and usually results in an improvement in symptoms and in some cases, it is curative. Other forms of treatment include pharmacological interventions, positioning and nasopharyngeal intubation.
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The cardiovascular sequelae best shown to be associated with OSA are systemic hypertension and acute vascular events. The cardiovascular sequelae, including acute myocardial infarction or nocturnal angina may be contributed to by arterial vasospasm or clot formation in the area of an atheroma. Thus far there are no data showing that treatment of OSA eliminates vascular sequelae, but much evidence shows that chronic CPAP therapy may lower elevated blood pressure in some patients. However, for a variety of reasons mentioned above, CPAP does not correct hypertension in all OSA patients.