Congestive heart failure and obstructive sleep apnea: Difference between revisions
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==Effect of [[CPAP]] in [[HFrEF]]== | ==Effect of [[CPAP]] in [[HFrEF]]== | ||
* Use of nocturnal [[continuous positive airway pressure]] [[CPAP]] in [[OSA]] and [[HFrEF]] was associated with reduced central [[sympathetic]] [[vasoconstrictor]] outflow and improve [[vagal]] modulation of the [[heart]] by increasing high-frequency [[heart rate]] | * Use of nocturnal [[continuous positive airway pressure]] [[CPAP]] in [[OSA]] and [[HFrEF]] was associated with reduced central [[sympathetic]] [[vasoconstrictor]] outflow and improve [[vagal]] modulation of the [[heart]] by increasing high-frequency [[heart rate variability]].<ref name="pmid15963401">{{cite journal |vauthors=Usui K, Bradley TD, Spaak J, Ryan CM, Kubo T, Kaneko Y, Floras JS |title=Inhibition of awake sympathetic nerve activity of heart failure patients with obstructive sleep apnea by nocturnal continuous positive airway pressure |journal=J Am Coll Cardiol |volume=45 |issue=12 |pages=2008–11 |date=June 2005 |pmid=15963401 |doi=10.1016/j.jacc.2004.12.080 |url=}}</ref> | ||
==References== | ==References== | ||
Revision as of 15:03, 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 with effects on cardiovascular system by increasing the risk of hypertension, coronary artery disease, cardiac arrhythmias, sudden cardiac death, and heart failure. Obstructive sleep apnea contributes to the development and progression of HF. Hypoxia caused activation of inflammatory pathway leading to endothelial damage, atherogenesis, and heart failure. Activate profibrotic transforming growth factor-β during inflammatory process may cause 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.[1]
- 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, CD32.
- Activate inflammatory pathways can lead to endothelial damage, atherogenesis, and heart failure.
- Activate profibrotic transforming growth factor-β during inflammatory process leads to increased deposition of extracellular matrix and consequent myocardial fibrosis, and to worsening LV diastolic function.
- Common risk factors of OSA in patients with HFrEF include older age, male sex, higher BMI, and habitual snoring.[2]
- In patients with HFrEF and HFpEF, OSA is more prevalent than in the general population.
- Predictors of risk OSA and CSA in HFrEF are atrial fibrillation, ventricular arrhythmias, lower LV ejection fraction (LVEF, and higher levels of serum brain natriuretic peptide (BNP), endothelin-1, and urinary norepinephrine.[2][3][4][3]
Effect of CPAP in HFrEF
- Use of nocturnal continuous positive airway pressure CPAP in OSA and HFrEF was associated with reduced central sympathetic vasoconstrictor outflow and improve vagal modulation of the heart by increasing high-frequency heart rate variability.[5]
References
- ↑ Yu AY, Shimoda LA, Iyer NV, Huso DL, Sun X, McWilliams R, Beaty T, Sham JS, Wiener CM, Sylvester JT, Semenza GL (March 1999). "Impaired physiological responses to chronic hypoxia in mice partially deficient for hypoxia-inducible factor 1alpha". J Clin Invest. 103 (5): 691–6. doi:10.1172/JCI5912. PMC 408131. PMID 10074486.
- ↑ 2.0 2.1 Yumino D, Wang H, Floras JS, Newton GE, Mak S, Ruttanaumpawan P, Parker JD, Bradley TD (May 2009). "Prevalence and physiological predictors of sleep apnea in patients with heart failure and systolic dysfunction". J Card Fail. 15 (4): 279–85. doi:10.1016/j.cardfail.2008.11.015. PMID 19398074.
- ↑ 3.0 3.1 Vazir A, Hastings PC, Dayer M, McIntyre HF, Henein MY, Poole-Wilson PA, Cowie MR, Morrell MJ, Simonds AK (March 2007). "A high prevalence of sleep disordered breathing in men with mild symptomatic chronic heart failure due to left ventricular systolic dysfunction". Eur J Heart Fail. 9 (3): 243–50. doi:10.1016/j.ejheart.2006.08.001. PMID 17030014.
- ↑ Javaheri S (January 2006). "Sleep disorders in systolic heart failure: a prospective study of 100 male patients. The final report". Int J Cardiol. 106 (1): 21–8. doi:10.1016/j.ijcard.2004.12.068. PMID 16321661.
- ↑ Usui K, Bradley TD, Spaak J, Ryan CM, Kubo T, Kaneko Y, Floras JS (June 2005). "Inhibition of awake sympathetic nerve activity of heart failure patients with obstructive sleep apnea by nocturnal continuous positive airway pressure". J Am Coll Cardiol. 45 (12): 2008–11. doi:10.1016/j.jacc.2004.12.080. PMID 15963401.