Congestive heart failure and obstructive sleep apnea: Difference between revisions
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* Two types of [[hypopnea]] include [[obstructive]] or [[central]]. | * Two types of [[hypopnea]] include [[obstructive]] or [[central]]. | ||
==[[Pathophysiology]]== | |||
* [[Obstructive sleep apnea]] is characterized by recurrent [[pharyngeal ]] collapse during [[sleep]]. | * [[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]]. | * [[Hypopnea]] or [[apnea]] occurs in the presence of [[pharynx]] collapse upon normal withdrawal of [[pharyngeal]] [[dilator muscle]] tone during [[sleep]]. | ||
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* [[Obstructive sleep apnea]] leading to elevations in [[systemic blood pressure ]] ([[BP]]) secondary to [[hypoxia]], arousals from [[sleep]], and increased [[sympathetic nervous system]] activity ([[SNA]]). | * [[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]]. | * 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 with resultant systolic24–28 or diastolic29 dysfunction may also diminish oxygen delivery to the myocardium. Risks include myocardial ischemia, arrhythmias, and sudden cardiac death during sleep from the generation of free oxygen radicals and inflammation. Patients with OSA have low plasma nitrite concentrations and diminished endothelial-mediated vasodilation.30 Reactive oxygen species selectively activate inflammatory pathways by activating nuclear factor-kappa B (NFκB) rather than hypoxia-inducible factor-1 (HIF-1), the transcriptional regulator of the adaptive pathway.31 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 selectin, and CD15,32 that can lead to endothelial damage, atherogenesis, and HF. Infiltrating inflammatory cells activate profibrotic transforming growth factor-β, which leads to increased deposition of extracellular matrix and consequent myocardial fibrosis,33 and to worsening LV diastolic function | |||
==References== | ==References== | ||
Revision as of 07:25, 26 March 2022
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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. Common complications association obstructive sleep apnea include hypertension, coronary artery disease, cardiac arrhythmias, sudden cardiac death, and heart failure.
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 with resultant systolic24–28 or diastolic29 dysfunction may also diminish oxygen delivery to the myocardium. Risks include myocardial ischemia, arrhythmias, and sudden cardiac death during sleep from the generation of free oxygen radicals and inflammation. Patients with OSA have low plasma nitrite concentrations and diminished endothelial-mediated vasodilation.30 Reactive oxygen species selectively activate inflammatory pathways by activating nuclear factor-kappa B (NFκB) rather than hypoxia-inducible factor-1 (HIF-1), the transcriptional regulator of the adaptive pathway.31 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 selectin, and CD15,32 that can lead to endothelial damage, atherogenesis, and HF. Infiltrating inflammatory cells activate profibrotic transforming growth factor-β, which leads to increased deposition of extracellular matrix and consequent myocardial fibrosis,33 and to worsening LV diastolic function