Congestive heart failure and obstructive sleep apnea
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Resident Survival Guide |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Obstructive sleep apnea is a sleep-related breathing disorder that affects on cardiovascular function including hypertension, coronary artery disease, cardiac arrhythmias, sudden cardiac death, and heart failure. Hypoxia caused activation of inflammatory pathway can lead to endothelial damage, atherogenesis, and heart failure. Infiltrating inflammatory cells activate profibrotic transforming growth factor-β, which leads to increased deposition of extracellular matrix and consequent myocardial fibrosis and worsening LV diastolic function.
Sleep apnea in heart failure disease
- Sleep apnea is defined as partial or complete cessation of breathing during night-time sleep, resulting in repeated arousal from sleep, oxyhemoglobin desaturation, and daytime sleepiness.
- Apnea is as complete cessation of airflow for >10 s.
- Hypopnea, or partial cessation of airflow, is defined as a 50% to 90% reduction in airflow for >10 s, and >3% decrease in oxyhemoglobin saturation (SaO2) terminated by arousal.
- The 3 types of apnea include central, obstructive, and mixed.
- Central sleep apnea (CSA) is characterized by a complete withdrawal of central respiratory drive to the inspiratory muscles, including the diaphragm, and results in the simultaneous absence of naso-oral airflow and thoracoabdominal excursions.
- In obstructive sleep apnea (OSA), the thoracic inspiratory muscles, including the diaphragm, are active, so thoracoabdominal excursions are seen.
- Absence of airflow results from upper-airway occlusion caused by lost pharyngeal dilator muscle tone, with consequent pharyngeal collapse.
- Mixed apnea has an initial central component followed by an obstructive component.
- Two types of hypopnea include obstructive or central.
Pathophysiology
- Obstructive sleep apnea is characterized by recurrent pharyngeal collapse during sleep.
- Hypopnea or apnea occurs in the presence of pharynx collapse upon normal withdrawal of pharyngeal dilator muscle tone during sleep.
- Obesity and fat deposition around the pharynx are responsible of pharyngeal narrowing.
- Edema of the peripharyngeal when lying asleep due to leg fluid displacement during the day predisposing the individual to OSA.
- Obstructive sleep apnea causes a drop in intrathoracic pressure, hypoxia, and arousal.
- The drop in intrathoracic pressure increases left ventricular (LV) transmural pressure, and afterload.
- This drop in pressure increases venous return, causing right ventricular distention and a leftward shift of the interventricular septum and consequent decreased LV filling.
- Decreased LV filling and increased afterload lead to reduced stroke volume.
- Obstructive sleep apnea leading to elevations in systemic blood pressure (BP) secondary to hypoxia, arousals from sleep, and increased sympathetic nervous system activity (SNA).
- The combination of increased LV afterload and increased heart rate secondary to augmented SNA leads to myocardial oxygen supply/demand mismatch, cardiac ischemia and arrhythmias, LV hypertrophy, LV enlargement, and HF.
- Rapid-eye-movement (REM) sleep constitutes 20% to 25% of sleep and is associated with short surges of sympathetic activity.
- Sleep generally is a period of increased vagal activity and slower heart rates and lower BP. However, arousals after disordered breathing events in OSA leading to increase sympathetic nerve activity and risk of HF disease.
- Hypoxemia caused systolic and diastolic dysfunction may also lessen oxygen delivery to the myocardium.
- Increased free oxygen radicals and inflammation may cause myocardial ischemia, arrhythmias, and sudden cardiac death.
- Plasma nitrite concentrations, and endothelial-mediated vasodilation decrease in patients with OSA.
- Reactive oxygen species selectively activate inflammatory pathways.
- Activation of NFκB leads to increased production of tumor necrosis factor-α, interleukin-6, interleukin-8, and C-reactive protein, as well as adhesion molecules such as intracellular and vascular cell adhesion molecules, E selecting, and CD15,32.
- Activate inflammatory pathways can lead to endothelial damage, atherogenesis, and heart failure.
- Infiltrating inflammatory cells activate profibrotic transforming growth factor-β, which leads to increased deposition of extracellular matrix and consequent myocardial fibrosis, and to worsening LV diastolic function.