Obstructive sleep apnoea - mechanism of associated hypertension
Core concept
- Dominant mechanism: intermittent hypoxia -> peripheral chemoreflex -> sustained sympathetic overactivity
- Apnoea -> hypoxia + hypercapnia -> carotid body chemoreceptor activation
- -> inc central sympathetic outflow (confirmed directly by muscle sympathetic nerve activity recordings)
- -> vasoconstriction, inc HR, BP surges of 30-60 mmHg at each arousal
- Chemoreflex sensitisation makes the drive persist into wakefulness -> daytime hypertension
- This is the answer the exam wants: it is not mechanical, and it is not simply obesity
- Supporting mechanisms
- Loss of nocturnal dipping -> non-dipper or reverse-dipper pattern
- RAAS activation and aldosterone-mediated fluid retention -> rostral fluid shift worsens upper airway collapse (a vicious cycle)
- Endothelial dysfunction - dec NO, inc endothelin-1; oxidative stress from hypoxia-reoxygenation (reperfusion-injury physiology)
- Systemic inflammation - inc CRP, IL-6, TNF-alpha; inc platelet activation
- Large negative intrathoracic pressure (-40 to -80 cmH2O) against a closed airway (Mueller manoeuvre) -> inc LV transmural pressure and afterload, inc venous return, atrial stretch -> AF
3 more sections, plus exam facts
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