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Sleep Apnea- Multidisciplinary/Holistic perspective
- 1. Sleep Apnea: BeyondSleep Disruption – A Holistic Perspective Presented by: | Date:
- 2. Sleep Apnea –The Silent Epidemic 936 million 15% 80% Estimated global burden People have clinically significant OSA (AHI >5/hr) Moderate-to-severe OSA remains undiagnosed. Types • Obstructive (OSA) • Central (CSA) • Complex Sleep Apnea (CompSAS). 🧠 Clinical Insight: Undiagnosed OSA often masquerades as resistant hypertension, depression, or chronic fatigue. Clinicians must maintain a high index of suspicion. Benjafield AV, et al. Estimation of the global prevalence and burden of obstructive sleep apnoea. Lancet Respir Med. 2019;7(8):687–698. Driven by – • Obesity, • Aging • Metabolic comorbidities
- 3. OSA is anindependent and modifiable risk factor for cardiovascular disease (CVD), including: ▪ Hypertension ▪ Coronary artery disease ▪ Atrial fibrillation (AF) ▪ Stroke ▪ Heart failure Magnitude of Risk: •140%↑ risk of heart failure •60% ↑ risk of stroke •30% ↑ risk of coronary artery disease OSA and Cardiovascular Disease: An Independent Risk Factor Javaheri S, et al. Sleep apnea and cardiovascular disease. Circulation. 2016;133(4):e17–e47.
- 4. OSA and CardiovascularDisease: An Independent Risk Factor Mechanisms: • Intermittent hypoxia → ↑ sympathetic activity • Sleep fragmentation → BP variability • Endothelial dysfunction, oxidative stress, and arterial stiffness • Inflammatory cytokine release → vascular remodeling Circulation. 2008;118:1080–1111 •.
- 5. OSA and CardiovascularDisease: An Independent Risk Factor Sánchez-de-la-Torre, Manuel et al. The Lancet Respiratory Medicine, Volume 1, Issue 1, 61 - 72
- 6. OSA and CardiovascularDisease: An Independent Risk Factor •Nocturnal hypertension and a non-dipping BP pattern are hallmarks of OSA, often missed on routine clinic measurements. •The Sleep Heart Health Study and Wisconsin Sleep Cohort established the dose-response relationship between OSA severity (AHI) and CVD risk, independent of BMI. •Left atrial enlargement, commonly seen in patients with OSA, can predispose to AF and worsen its recurrence post-ablation 🧠 Case Nugget: A 57-year-old male with drug-refractory hypertension and new-onset paroxysmal AF is referred for evaluation. Overnight oximetry shows desaturation; PSG confirms severe OSA (AHI 42/hr). Post- CPAP, his BP normalizes, and AF burden reduces on Holter at 3 months. 💡 Implication: OSA screening should be part of routine cardiovascular risk stratification — especially in patients with resistant hypertension or arrhythmias. Marin JM, et al. Long-term cardiovascular outcomes in men with obstructive sleep apnoea–hypopnoea with or without treatment with CPAP: an observational study. Lancet. 2005;365(9464):1046–1053 Young T, et al. Sleep-disordered breathing and cardiovascular disease. JAMA. 2008;300(23):2751–2759. Am J Respir Crit Care Med Vol 163. pp 19–25, 200
- 7. Sleep Apnea andChronic Kidney Disease (CKD): A Two-Way Street Bidirectional Relationship: • OSA can accelerate CKD progression. • CKD contributes to the severity and development of OSA. How OSA Affects CKD: • Intermittent hypoxia → renal ischemia and oxidative stress • ↑ Sympathetic tone → glomerular hyperfiltration and hypertension • ↑ Risk of albuminuria and faster decline in eGFR How CKD Affects OSA: • Fluid overload → rostral fluid shift → pharyngeal narrowing during sleep • Uremia → impaired respiratory control and ventilatory response Current Sleep Medicine Reports (2020) 6:85–93
- 8. Sleep Apnea andChronic Kidney Disease (CKD): A Two-Way Street • Many CKD patients attribute fatigue to uremia — but in reality, sleep apnea may be the silent contributor. • Fluid shifts, especially when patients lie supine, worsens pharyngeal obstruction. • There’s also early evidence linking OSA to increased renal sympathetic nerve activity, compounding hypertension. • Diagnosing OSA early in CKD may slow GFR decline, reduce BP meds, and improve QoL. • AHI severity correlates with proteinuria levels in observational studies. • For patients on dialysis, untreated OSA is linked to higher cardiovascular mortality. Lin CH, Perger E, Lyons OD. Obstructive sleep apnea and chronic kidney disease. Curr Opin Pulm Med. 2018 Nov;24(6):549-554 🧠 Case Nugget: 65-year-old male on maintenance hemodialysis reports persistent fatigue and poor sleep. Overnight pulse oximetry reveals desaturation with frequent apneic spells. PSG confirms severe OSA. CPAP initiated → improved morning BP and alertness. eGFR decline stabilizes over 6 months. 💡 Implication: Suspect OSA in dialysis or pre-dialysis patients with excessive daytime sleepiness, refractory hypertension, or volume overload despite adherence.
- 9. OSA and LungDiseases – The Overlap Syndrome Overlap Syndrome = Coexistence of Obstructive Sleep Apnea (OSA) and Chronic Respiratory Disease Especially prevalent in Chronic Obstructive Pulmonary Disease (COPD) and Interstitial Lung Diseases (ILDs) Prevalence: • OSA in COPD: ~44% • OSA in ILDs (e.g. IPF): Up to 88% Cleveland Clinic Journal of Medicine February 2016, 83 (2) 127-140
- 10. Protective and promotingfactors for overlap syndrome development Pathophysiological interactions between COPD and OSA predisposing to cardiovascular disease OSA and Lung Diseases – The Overlap Syndrome Breathe 2022 18(3): 220073
- 11. OSA and LungDiseases – The Overlap Syndrome • Those with COPD or ILD are at high risk of undiagnosed OSA. • In ILDs like IPF, OSA contributes to microvascular pulmonary changes and worsens nocturnal desaturation, which may appear disproportionate to daytime function. • In COPD, OSA exacerbates hypercapnia, right heart strain, and can increase hospitalizations. • CPAP therapy in these patients can improve sleep quality, reduce exacerbations, and may improve survival when appropriately applied. • BiPAP (not just CPAP) may be needed in overlap patients with significant hypoventilation. Sunwoo, B. Y., Raphelson, J. R., & Malhotra, A. (2024). Chronic obstructive pulmonary disease and obstructive sleep apnea overlap: who to treat and how? Expert Review of Respiratory Medicine, 18(7), 527–537.
- 12. Clinical Impact: • Moreprofound nocturnal hypoxemia and hypercapnia • ↑ Risk of pulmonary hypertension and right heart strain • Reduced quality of life and exercise tolerance • ↑ Mortality compared to OSA or lung diseases alone OSA and Lung Diseases – The Overlap Syndrome 🧠 Case Nugget: A 63-year-old female with stable IPF complains of worsening fatigue and poor sleep. Despite nocturnal oxygen use, desaturations persist. PSG reveals moderate OSA. CPAP added to oxygen therapy → improved fatigue and nocturnal saturation stability. 💡 Implication: Overlap syndrome is often masked. Suspect OSA in lung disease patients with unexplained fatigue, desaturation despite oxygen, or PH. Screening and treating OSA can significantly alter the disease trajectory. Lancaster LH, et al. Obstructive sleep apnea is common in idiopathic pulmonary fibrosis. Chest. 2009;136(3):772–778.
- 13. PAP Therapies –The Cornerstone of Treatment Current Pulmonology Reports 12(2):1-8
- 14. • Pulmonologists mustbe active participants in selecting, titrating, and troubleshooting PAP therapy. • CPAP is not one-size-fits-all and early discomfort or nonadherence often stems from poor device or mask matching. • APAP is ideal for patients with positional or REM- predominant OSA. • BiPAP is underused in overlap syndrome, particularly useful for those with CO₂ retention or restrictive lung disease. • ASV has been a game-changer for central apnea, yet contraindicated in HFrEF patients post SERVE-HF trial. PAP Therapies – The Cornerstone of Treatment 🧠 Case Nugget: A 52-year-old male with AHI 39/hr and poor sleep compliance is intolerant to CPAP due to pressure intolerance. Shifted to APAP with ramp features → improved comfort and >6 hrs/night use. Daytime fatigue resolved 💡 Implication: PAP type selection should be tailored. Early mask fitting and titration strategy directly influence long-term adherence. Current Pulmonology Reports 12(2):1-8
- 15. Lifestyle Measures • Weightloss, regular exercise, positional therapy • Avoid alcohol, sedatives, and supine sleep • Bariatric surgery: improves or resolves OSA in select obese patients Oral Appliances (OAs) • Mandibular advancement devices (MADs) reposition the jaw to open the airway • Effective for mild-to-moderate OSA or PAP- intolerant patients • Requires dental evaluation and customization Beyond PAP – Adjunctive and Emerging Treatments Verbraecken J, Dieltjens M, Op de Beeck S, Vroegop A, Braem M, Vanderveken O, Randerath W. Non-CPAP therapy for obstructive sleep apnoea. Breathe (Sheff). 2022 Sep;18(3):220164.
- 16. Surgical Options • Uvulopalatopharyngoplasty(UPPP): Removes/repositions soft tissue • Maxillomandibular advancement: Skeletal expansion of the airway • DISE-guided surgery improves target site selection Beyond PAP – Adjunctive and Emerging Treatments Neuromodulation • Hypoglossal Nerve Stimulation (HNS): Implanted device activates tongue muscles to maintain airway patency Ideal for patients with AHI 15–65, BMI <32, PAP intolerance • Other Devices (Investigational): EPAP valves Oral negative pressure devices Verbraecken J, Dieltjens M, Op de Beeck S, Vroegop A, Braem M, Vanderveken O, Randerath W. Non-CPAP therapy for obstructive sleep apnoea. Breathe (Sheff). 2022 Sep;18(3):220164.
- 17. Beyond PAP –Adjunctive and Emerging Treatments Abid R, Zhang L, Bhat A. Non-CPAP Therapies for Obstructive Sleep Apnea in Adults. Mo Med. 2024 Sep-Oct;121(5):385-390.
- 18. Beyond PAP –Adjunctive and Emerging Treatments • It is essential to break the misconception that CPAP or nothing is the treatment paradigm. • Many patients, especially those with mild-to-moderate OSA, anatomical variation, or CPAP intolerance benefit from alternatives. • MADs have strong evidence and high patient satisfaction when fitted properly. • HNS (Inspire device) offers a non-CPAP, non-surgical solution with growing evidence from randomized trials (STAR trial). • Bariatric surgery is effective not just for OSA severity but also for reversing related comorbidities, though relapse is possible if weight returns. • Positional therapy (e.g. lateral sleep training) is effective in positional OSA (supine AHI > 2× non-supine AHI). • Encourage you to adopt a multi-modal, shared decision- making approach tailored to patient phenotype and preferences. 🧠 Case Nugget: A 48-year-old woman with BMI 27 and mild OSA (AHI 11/hr) is unable to tolerate CPAP. Fitted with a custom MAD → 70% reduction in AHI, improved sleep, no desaturation events on repeat HSAT. 💡 Implication: Not all OSA needs CPAP. Patient-centric treatment pathways—especially in mild cases—can improve adherence and outcomes. Breathe 2022 18(3): 220164
- 19. Advantages: • Performed inthe patient’s natural sleep environment • Cost-effective and accessible; avoids waitlists for lab- based PSG • Facilitates early diagnosis in resource-limited or rural settings Limitations: • Lacks EEG → cannot quantify total sleep time → may underestimate AHI • Inadequate in patients with: ▪ CHF, CRD, stroke, neuromuscular disease ▪ Morbid obesity (BMI >40–50) ▪ High suspicion but negative/inconclusive HSAT • Cannot detect other sleep disorders (e.g. PLMD, parasomnias) HSAT – Balancing Convenience and Accuracy Indian Journal of Sleep Medicine (2022): 10.5005/jp-journals-10069-0106
- 20. HSAT – BalancingConvenience and Accuracy Indian Journal of Sleep Medicine (2022): 10.5005/jp-journals-10069-0106
- 21. HSAT – BalancingConvenience and Accuracy Practical Considerations: • Ideal for adults with high pre-test probability of moderate- to-severe OSA and without significant comorbidities • Negative HSAT with ongoing clinical suspicion → full PSG is required • While HSAT has revolutionized access, we must interpret its findings in clinical context. AHI underestimation is common, particularly in short sleepers, fragmented sleep, or REM-predominant apnea. • The distinction between Type III devices (no EEG) vs. Type II/PSG should be clear • Technically inadequate HSATs occur in up to 20% of cases and need retesting or lab studies. • HSAT is not appropriate in patients with unstable cardiopulmonary disease or suspected comorbid sleep disorders. • Portable multi-channel testing (Type II) is being piloted in some centers as a hybrid solution. 🧠 Case Nugget: HSAT in a 60-year-old male with BMI 42 and witnessed apneas was reported as normal (AHI 3/hr). Repeat in-lab PSG showed severe OSA (AHI 28/hr). CPAP was initiated → dramatic improvement in symptoms. 💡 Implication: HSAT may miss events in high-risk phenotypes. Know when to escalate to full PSG, especially in obese, cardiac, or neurologically complex patients. Hussein O, Alkhader A, Gohar A, Bhat A. Home Sleep Apnea Testing for Obstructive Sleep Apnea. Mo Med. 2024 Jan-Feb;121(1):60-65
- 22. Prevalence of secondarycauses of hypertension associated with resistant hypertension. OSA indicates obstructive sleep apnea. OSA in Resistant Hypertension and Atrial Fibrillation Hypertension. 2011 Nov;58(5):811-7.
- 23. • OSA isthe most common secondary cause of RHTN • Prevalence: 70–90% of RHTN patients have undiagnosed OSA • Pathophysiology: ▪ ↑ Sympathetic tone ▪ RAAS activation ▪ Arterial stiffness and non-dipping BP pattern • CPAP improves 24-hr BP control, especially nocturnal BP Azizi M, Amar L, Lorthioir A. Resistant Hypertension and Obstructive Sleep Apnea: Is There a Specific Indication for Endovascular Renal Denervation? Hypertension. 2018 Aug;72(2):281-282. OSA in Resistant Hypertension and Atrial Fibrillation
- 24. OSA in ResistantHypertension and Atrial Fibrillation After adjustment for body mass index, neck circumference (neck circ), hypertension, and diabetes mellitus, AF is significantly associated with OSA Prevalence of OSA is significantly higher in patients with AF than in patients without past or current AF in general cardiology practice Gami AS, Pressman G, Caples SM, Kanagala R, Gard JJ, Davison DE, Malouf JF, Ammash NM, Friedman PA, Somers VK. Association of atrial fibrillation and obstructive sleep apnea. Circulation. 2004 Jul
- 25. OSA in ResistantHypertension and Atrial Fibrillation • OSA is an independent risk factor for incident and recurrent AF • Prevalence of OSA in AF patients: 21– 74% • Mechanisms: ▪ Intermittent hypoxia → atrial remodeling ▪ ↑ Intrathoracic pressure swings ▪ Autonomic instability and inflammation • CPAP therapy reduces AF recurrence post-ablation Linz, B., Norup Hertel, J., Hendriks, J., Saljic, A., Dobrev, D., Baumert, M., … Linz, D. (2022). Sle apnea and atrial fibrillation: challenges in clinical and translational research. Expert Review o Cardiovascular Therapy, 20(2), 101–109.
- 26. 🧠 Case Nugget: 54-year-oldman with RHTN on four antihypertensives and paroxysmal AF presents with daytime fatigue. PSG reveals severe OSA (AHI 47/hr). After 8 weeks of CPAP use, BP normalized, and AF burden reduced on Holter. 💡 Implication: Always screen for OSA in patients with RHTN or recurrent AF. Treating sleep apnea can directly impact arrhythmia control and medication burden. Expert Review of Cardiovascular Therapy, 20(2), 101–109. OSA in Resistant Hypertension and Atrial Fibrillation
- 27. Conclusion – TowardsHolistic Sleep Apnea Management • Think Beyond Snoring OSA is a systemic disease—screen in AF, RHTN, ILD, CKD, and fatigue with no clear cause. • One Size Doesn’t Fit All PAP is powerful, but alternatives like MADs, HNS, and lifestyle therapy matter; match treatment to phenotype. • Don’t Stop at HSAT Home testing is helpful but limited, escalate when suspicion persists or results are borderline. • Make Sleep Multidisciplinary Partner with ENT, cardiology, nephrology, and dental sleep experts for better outcomes. • Own the Follow-up Use tech, track adherence, coach behavior—managing OSA doesn’t end at diagnosis.
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Editor's Notes
- #2 Emphasize that OSA is not just a sleep disorder but a systemic condition. Undiagnosed OSA is common even in tertiary care. This is especially true in women, elderly patients, and those with obesity or multiple comorbidities. OSA should be considered in patients with metabolic syndrome, unexplained fatigue, or treatment-resistant hypertension.
- #3 OSA contributes to cardiovascular morbidity through a cascade of sympathetic activation, vascular remodeling, and systemic inflammation. Even after adjusting for BMI and age, the risk remains elevated. The Sleep Heart Health Study and Wisconsin Cohort support this.
- #4 OSA contributes to cardiovascular morbidity through a cascade of sympathetic activation, vascular remodeling, and systemic inflammation. Even after adjusting for BMI and age, the risk remains elevated. The Sleep Heart Health Study and Wisconsin Cohort support this.
- #5 We start on the left with classic features of OSA: Obstructive episodes during sleep cause intermittent oxygen desaturation (seen in the SaO₂ graph), Along with cortical arousals that fragment sleep, and Intrathoracic pressure changes due to effort against a closed airway—picked up on polysomnography (flow, chest, abdomen tracings). These lead to chronic activation of harmful physiological pathways (center column): Sympathetic overactivity — persistent catecholamine surges raise blood pressure and heart rate. Endothelial dysfunction — promotes atherogenesis. Inflammation and oxidative stress — fuel cardiovascular remodeling. Metabolic dysregulation and hypercoagulability — increase the risk of thrombotic events. Moving to the right side, the end-organ consequences include: Systemic hypertension — often nocturnal and non-dipping, Arrhythmias, especially atrial fibrillation and ventricular ectopy, Heart failure — especially right heart strain in overlap syndromes, Stroke and myocardial infarction, and in severe cases, Sudden cardiac death, particularly during REM sleep when OSA is most pronounced. You may want to emphasize that these mechanisms operate silently and chronically, often in patients who don’t meet the “classic” OSA phenotype. 🩺 Clinical Reinforcement: This pathophysiology underscores why OSA should be suspected in patients with: Resistant hypertension, Recurrent AF post-ablation, Nocturnal angina or cardiac events, Unexplained fatigue or cognitive decline.
- #7 Pulmonologists must consider renal implications of untreated OSA. CKD patients often attribute fatigue to uremia. However, sleep apnea frequently coexists and exacerbates renal hypoxia and blood pressure variability.
- #9 This is a critical pulmonology slide. Many CRD patients are never evaluated for OSA despite significant overlap. Overlap syndrome leads to higher cardiovascular and respiratory mortality. BiPAP may be preferred in cases with hypercapnia.
- #10 This slide addresses the complex interplay between COPD and OSA, a combination known as Overlap Syndrome, which significantly worsens patient outcomes—especially cardiovascular risk. 🔹 On the left, we see factors that influence overlap development: Promoting factors: ▪ Use of steroids (oral/inhaled) ▪ Rostral fluid shift during sleep ▪ Smoking — a shared risk for both diseases Protective factors: ▪ Lung hyperinflation (mechanical splinting effect) ▪ Lower BMI ▪ Reduced REM sleep ▪ Theophylline therapy (stimulates respiration) This illustrates why not all COPD patients develop OSA, and vice versa. 🔹 On the right, we zoom into the shared pathophysiological pathway that makes this overlap so dangerous: OSA and COPD share common risk factors: obesity and smoking. Both contribute to chronic hypoxia, which triggers: ▪ Oxidative stress ▪ Increased inflammatory mediators ▪ Sympathetic overactivation These feed into endothelial dysfunction and plaque formation, ultimately increasing the risk of cardiovascular disease. 🩺 Clinical Takeaway: Patients with overlap syndrome have more severe nocturnal desaturation and are at higher risk for pulmonary hypertension, right heart failure, and sudden cardiac events. Screen aggressively and consider BiPAP or nocturnal oxygen + CPAP strategies for management.
- #13 This slide compares the four major types of Positive Airway Pressure (PAP) therapies, each tailored to different OSA phenotypes and comorbidities. CPAP is the first-line therapy for uncomplicated OSA. It's simple, inexpensive, but often poorly tolerated due to fixed pressure. APAP adjusts pressure based on resistance—ideal for patients with positional or REM-related OSA and those who can't tolerate fixed CPAP. BiPAP delivers higher inspiratory pressure—especially useful in CO₂ retainers, neuromuscular weakness, or overlap syndrome. ASV is reserved for complex cases (e.g., central apneas or Cheyne–Stokes in CHF), but should be avoided in HFrEF with low EF. Tip: Focus on comfort, comorbidities, and pressure needs when deciding. Patient education and early follow-up are critical for long-term adherence.
- #20 This algorithm helps determine when to use in-lab polysomnography (PSG) versus home sleep apnea testing (HSAT). 🔹 Start with risk stratification: If the patient is a mission-critical worker (e.g., airline pilot), or has suspected central sleep apnea (CSA) or hypoventilation, they must go for full in-lab PSG—no shortcuts. 🔹 For typical OSA: If symptoms suggest moderate to severe OSA (EDS + ≥2: snoring, witnessed apneas, hypertension), in-lab PSG is preferred. If mild OSA is suspected and there are no red flags, HSAT is acceptable. 🔹 Avoid HSAT in patients with: COPD or other chronic respiratory diseases Hypoventilation syndromes (OHS, neuromuscular) CHF Stroke or TIA Opioid use 🔹 If HSAT is inconclusive, move to in-lab PSG.
- #22 This chart drives home a critical clinical point: Obstructive Sleep Apnea (OSA) is the most common secondary cause of resistant hypertension, present in 64% of such cases—far more than other commonly screened causes like: Primary aldosteronism (5.6%) Renal artery stenosis (2.4%) Thyroid disease, oral contraceptives, renal parenchymal disease—all <2% 🔹 And yet, OSA is often the least screened in real-world practice. 🔹 In atrial fibrillation (AF), especially post-ablation, untreated OSA significantly increases the risk of recurrence. 💡 Practical Takeaway: Any patient on ≥3 antihypertensives—including a diuretic—should be evaluated for OSA, particularly if they also report snoring or daytime fatigue. Also, screen all AF patients for OSA pre-ablation. This is low-hanging fruit where pulmonologists can lead cross-specialty collaboration with cardiology and internal medicine.
- #23 This slide explains why OSA is the most common secondary cause of resistant hypertension (RHTN)—often missed. 🔹 Up to 90% of RHTN patients may have undiagnosed OSA. 🔹 Mechanisms include: Recurrent hypoxia → ↑ sympathetic drive RAAS activation → vasoconstriction + fluid retention Non-dipping BP pattern due to disrupted sleep 🔹 Also note the contribution of nocturnal rostral fluid shift, especially in supine patients. 🔹 CPAP therapy has been shown to lower 24-hour BP—especially nocturnal values—improving cardiovascular outcomes. 💡 Reminder: Screen all patients with RHTN and AF—even if they don’t have classic OSA symptoms.
- #24 This slide highlights the strong association between OSA and atrial fibrillation (AF). In this study, OSA prevalence was significantly higher in AF patients compared to general cardiology patients (P=0.0004). Even after adjusting for BMI, neck circumference, hypertension, and diabetes, AF independently increased the odds of having OSA (OR 2.19, P=0.0006). 🔹 In clinical practice, this means: Any patient with AF—especially if recurrent or post-ablation—should be screened for OSA, regardless of body habitus.
- #25 This schematic shows the chain reaction triggered by a single obstructive apnea event and how it promotes atrial fibrillation: Upper airway obstruction leads to ineffective inspiratory effort against a closed airway, generating large negative intrathoracic pressures. This causes intermittent hypoxia and hypercapnia, which activate the sympathetic nervous system and increase oxidative stress. These fluctuations alter atrial electrophysiology—affecting ERP (effective refractory period) and action potential duration—leading to atrial fibrosis and substrate remodeling. Over time, this repeated stress contributes to chronic atrial enlargement, setting the stage for persistent or recurrent AF. The visual helps bridge the mechanical events of OSA with electrophysiologic remodeling, reinforcing why managing OSA can modify AF outcomes.
- #26 This flowchart outlines a pragmatic approach to identifying undiagnosed OSA in patients with atrial fibrillation. 🔹 It starts with clinical suspicion—based on both patient history (like snoring or nocturnal symptoms) and clinical features (such as obesity, male gender, non-dipping hypertension, or difficult-to-control AF). 🔹 If OSA probability is high: Overnight oximetry is used as a quick, accessible screening step. If still suspicious, move to overnight polygraphy for confirmation. 🔹 If initial probability is low, but AF persists or escalates, a re-evaluation is recommended—this ensures we don’t miss evolving sleep-disordered breathing. 🔹 Once diagnosed, OSA treatment is initiated, ideally improving both AF control and cardiovascular outcomes.
- #27 Summarize that OSA is systemic. Pulmonologists must act as coordinators, not just diagnosticians. Mention integrated care models and digital health tools as the future. Reinforce shared decision-making.