The Pathophysiology of Sleep Apnoea: What We have Learned from Animal Models of Chronic Intermittent Hypoxia

Abstract

Sleep apnoea is a common condition associated with significant morbidity and mortality. The English bulldog is the only animal known to have sleep apnoea. In recent years, a number of animal models have been developed which have contributed greatly to our knowledge of the condition. These models develop a number of pathophysiological changes similar to human sleep apnoea such as systemic and pulmonary hypertension, increased haematocrit, and effects on blood coaguability, cardiac rhythmogenesis and central nervous system and upper airway muscle function. This review will describe what has been learned from these models concerning the pathophysiology of sleep apnoea with special emphasis on the role played by intermittent hypoxia.

Etiopathogenetic Mechanisms of Pulmonary Hypertension in Sleep-Related Breathing Disorders

“…Conversely, pulmonary vasoconstriction is a direct response to alveolar hypoxia in a physiologic attempt to minimize ventilation perfusion mismatch. The recurrence of hypoxemic episodes in sleep apnea result in repetitive increases in pulmonary artery pressures; however, about 1 in 5 patients develops sustained pulmonary hypertension during the daytime [ 66 – 70 ]. More severe OSA and hypoxia may lead to right ventricular hypertrophy culminating in daytime pulmonary hypertension and right ventricular failure in the presence of hypercapnia and chronic alveolar hypoventilation [ 71 – 74 ].…”