Sleep and CV System
During non-REM sleep, what happens to HR and BP?
They decrease (parasympathetic predominance).
Additional possible answers: ↓ cardiac output, ↓ sympathetic tone.
*Explanation: Parasympathetic (vagal) activity dominates in non-REM → lowering HR, BP, and metabolic demand, giving the CV system a nightly rest.
What are the two hallmark features of OSA?
Intermittent hypoxia and sleep fragmentation.
Additional possible answers: Repeated airway collapse, arousals.
*Explanation: OSA = recurrent airway obstruction → hypoxia-reoxygenation cycles (oxidative stress) + arousals (sleep fragmentation).
Which arrhythmia is most strongly linked with OSA?
Atrial fibrillation.
Additional possible answers: Bradyarrhythmias, ventricular ectopy, sudden cardiac death.
*Explanation: Hypoxia, atrial stretch, and surges in sympathetic activity increase AF risk. OSA is an independent risk factor for AF recurrence.
Why do OSA patients develop pulmonary hypertension?
Chronic hypoxia → pulmonary vasoconstriction.
Additional possible answers: Endothelial dysfunction, right heart strain.
*Explanation: Hypoxia triggers pulmonary vasoconstriction; sustained → pulmonary hypertension and cor pulmonale.
Which sleep stage causes surges in HR and BP?
REM sleep.
Additional possible answers: Sympathetic activation, CV variability.
*Explanation: REM is marked by bursts of sympathetic activity, leading to fluctuating HR and BP similar to waking levels.
What do negative intrathoracic pressure swings during OSA do?
Increase LV afterload and myocardial wall stress.
Additional possible answers: ↑ venous return, atrial stretch, mechanical stress.
*Explanation: Strong inspiratory effort against obstruction creates highly negative pressures → ↑ LV transmural pressure and preload/afterload load.
Why does OSA worsen heart failure?
↑ afterload, sympathetic drive, and structural remodeling.
Additional possible answers: Fluid shifts to airway at night, hypoxia-induced myocardial stress.
*Explanation: In HF, OSA raises ventricular wall stress and filling pressures, worsening both HFrEF and HFpEF.
Why do OSA patients lose the normal nocturnal BP dip?
Sleep fragmentation + sympathetic surges.
Additional possible answers: “Non-dipping” hypertension, persistent high BP.
*Explanation: Normally BP drops 10–20% at night. OSA prevents dipping, causing sustained hypertension and ↑ CV risk.
How does OSA contribute to the development of heart failure?
By increasing afterload, causing recurrent hypoxia, and sustaining sympathetic activation.
Additional possible answers: Neurohormonal activation (RAAS, catecholamines), cardiac remodeling.
*Explanation: OSA imposes hemodynamic stress (↑ LV wall stress), repeated oxygen desaturation, and sympathetic overdrive → these accelerate myocardial injury, LV hypertrophy, and eventual HF.
Why do OSA patients have persistent sympathetic activation?
Recurrent arousals and hypoxia cause sustained sympathetic drive.
Additional possible answers: ↑ catecholamines, hypertension, tachycardia.
*Explanation: Sympathetic surges at night “spill over” into daytime → loss of parasympathetic dominance, leading to hypertension and arrhythmia risk.
Why does OSA worsen ischemic heart disease?
Hypoxia ↓ O₂ supply, while pressure swings & sympathetic surges ↑ demand.
Additional possible answers: Nocturnal angina, MI risk, plaque instability.
*Explanation: Oxygen supply-demand mismatch increases angina frequency and accelerates CAD progression.
What vascular dysfunction is caused by intermittent hypoxia?
Endothelial dysfunction + arterial stiffness.
Additional possible answers: Accelerated atherosclerosis, impaired nitric oxide signaling.
*Explanation: Repeated hypoxia-reoxygenation cycles → oxidative stress, inflammation, and vascular remodeling → ↑ atherosclerosis and CV events.
How does OSA worsen prognosis in patients with established heart failure?
It increases hospitalisations, mortality, and arrhythmia risk.
Additional possible answers: Worsens EF (in HFrEF), elevates filling pressures (in HFpEF), induces pulmonary hypertension.
*Explanation: In HF patients, OSA amplifies pressure/volume loading and neurohormonal stress, leading to recurrent decompensations, arrhythmias (esp. AF, VT), and poorer survival.