Effects of sleep-disordered breathing on the respiratory system and cardio-respiratory control

Overview

Obstructive sleep apnoea (OSA) produces repeated cycles of hypoxia, hypercapnia, and arousal that drive measurable cardiovascular and respiratory control changes over time, independent of daytime sleepiness symptoms
OSA prevalence rises with obesity, and its cardiovascular consequences are a major driver of the excess morbidity/mortality associated with untreated moderate-severe disease

Repeated hypoxia/hypercapnia -> sympathetic surges -> sustained daytime hypertension, not just nocturnal BP elevation
Intrathoracic pressure swings against an occluded airway -> increased LV afterload -> long-term association with left ventricular hypertrophy, atrial fibrillation, and heart failure
Chronic intermittent hypoxia -> endothelial dysfunction, oxidative stress -> accelerated atherosclerosis
Chemoreceptor resetting from chronic intermittent hypoxia can blunt normal ventilatory responses over time

Polysomnography quantifies severity (AHI); cardiovascular risk assessment (BP, echocardiography if indicated) is part of the OSA workup given this bidirectional relationship

CPAP treatment reduces but does not fully normalise cardiovascular risk in severe OSA - treating OSA is part of, not a replacement for, standard cardiovascular risk management

Hypertension (especially resistant hypertension - screen for OSA), atrial fibrillation, heart failure, stroke

The cardiovascular consequences of OSA accumulate over years of untreated exposure - severity and duration both matter for cardiovascular risk, not just current symptom burden

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