Sleep Apnea and The Heart

Sleep Apnea and The Heart Joe of Pickwick Papers 1867 1979 Inventor of Continuous Positive Airway Pressure Therapy-Colin Sullivan First CPAP Mac...
Author: Ernest Bishop
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Sleep Apnea and The Heart

Joe of Pickwick Papers 1867

1979 Inventor of Continuous Positive Airway Pressure Therapy-Colin Sullivan

First CPAP Machine

Circulation Journal of the American Heart Association

NFL All Pro Linebacker

www.reggiewhitesleepdisordersfoundation.org

Growth in SDB Publications 6000 5000 4000 3000 2000 1000 0

Sleep Apnea and Heart Failure, JACC January 2011 ACCF/AHA Scientific Statement on Sleep Apnea and Cardiovascular Disease; Circulation, 2008. Sleep and Cardiovascular disease, Sleep Medicine

Clinics, 2007 Practice Parameters in Sleep Medicine; SLEEP, 2005. Sleep Disorders in Women, 2006.

K.D Weeks MD, FACC, FAASM The following relationships with commercial interests related to this presentation existed during the past 12 months: ResMed , Inc – Speaker

52 Yr. Old Male  HBP x 9 years. Referred By Anes thesiology for pre-op (“STOP”).

 LVH by Echo, EKG  New onset A.Fib  Resistant to multiple

Antihypertensive Drugs  Smokes and uses moderate alcohol  Erectile Dysfunction  Pulmonary Hypertension, 40-45 mmHg.

Upon Further Questioning  Neck Size 19 inches  BMI 33

 Mallampati Score of 4  Epworth Sleepiness Scale Score 16/24  One accident due to drowsy driving

 Wife : “His snoring will wake the dead.”

Pathophysiology of Apnea

Polysomnogram  Sleep Latency = 2.5 mins  REM Latency= 5.5 hours  Oxygen Sat Nadir= 74%  Apnea/Hypopnea Index= 66/hr.,

Supine, 43/hr on his side  Snoring= 8/10

 CPAP Trial on 8cm H2O-SUCCESSFUL!  AHI=0.0 and O2 Sat Nadir =89% (94% average)

 Snoring eliminated  ENT Evaluation: “Good candidate for

UPPP if he fails CPAP.”

Therapy  CPAP Therapy x 4 weeks = Satisfactory tolerance  “I feel less sleepy and my wife is happy.”

 Download chip: 78% compliance  No leak

Response  3 Months later: feels restored in AM.  Weight loss of 11 pounds

 Only on one antihypertensive drug  Romance has returned

Stats  20 Million Americans suffer from     

Sleep Apnea 80% are undiagnosed 15 Billion Dollar revenue base (up 300% according to MediCare) Estimates that 10% of those over 65 and 20% of those obese suffer from OSA Aging + Obesity + Diabetes + OSA = CAD, Afib, CHF, HBP, CVA “The worse your health, the worse you sleep. The worse you sleep, the worse your health.”

   

Cardiovascular Patients Heart and Wellness patients seeking preventive advice Pre-Op patients at Anesthesia Risk Research potential where few C-V Physicians now participate  Resolve Sleep Foundation’s demand that we diagnose and treat OSA patients in a more timely fashion/  Integrate a new service line into our comprehensive C-V management.  Improvement of fragmented approach to OSA and its Co-morbid conditions.

 OSA: Syndrome characterized by recurrent episodes of

complete upper airway obstruction (apnea), or partial obstruction (hypopnea), leading to disturbed nocturnal sleep and daytime hypersomnolence. Five or more respiratory events per hour is abnormal.  Apnea: Pause in breathing of 10 seconds or more.  Central Apnea: Pause in breathing due to absent chest or abdominal effort arising from central nervous system.  Hypopnea: Reduction in air flow of 10 seconds or more with or without arousal or oxygen desaturation.

 Related to increased sympathetic activation and decreased parasympathetic activity  HR  BP  O2 consumption  Afterload

Dysfunction created by Sleep Disordered Breathing Hypoxemia & reoxygenation Hypercapnea – hypocapnea Large negative swings in intrathoracic pressure, afterload, atrial transmural pressure leading to atrial stretch and A Fib, LVH Arousals cause sympathetic activation & parasympathetic activity HR, BP O2 Consumption, afterload

Nocturnal & Diurnal Hypertension  Decreases and increases in wall tension  Alterations in CBF  Adhesion molecules

 Inflammation  Transcription Factors  Oxidative Stress  Platelet aggregation/coagulopathy/thrombosis  Metabolic dysregulation

 Leptin resistance

 Endothelial Dysfunction

 Systemic Hypertension  Pulmonary Hypertension

 Systolic Heart Failure  Diastolic Heart Failure

 Arrhythmias  Atherosclerosis, CAD, CVA

 50% of OSA patients are hypertensive  30% of hypertensive patients have OSA

 Drug resistant hypertension = 83% have OSA  Non dippers have more OSA and higher 1.3 hazard ratio for mortality  LVH = non dipping  Mechanisms:

1. intermittent hypoxemia , 2. sympathetic stimulation, 3. renin angiotensin activation  Therapy with CPAP benefits hypertensives more than normal. Severe OSA = Most benefit  More studies needed

QUESTION? Which of the following statements regarding Heart Failure and Sleep Apnea is true? 1) There is a bidirectional relationship between HF and OSA. 2) Patients with HF and OSA generally deny excessive daytime sleepiness. 3) ABG’s of patients with HF patients usually show a low PCO2, due to hyperventilation, leaving them at the Apneic threshold of Central sleep apneic events. 4) Chronopharmacology , or well timed dosing of HF diuretic meds, can reduce OSA’s impact at bedtime 5) Obesity, HF, OSA, and hypoxemia predict an excess mortality rate. 6) All of the above.

 OSA seen in 37% of patients with systolic failure. Only

a minority have excessive daytime sleepiness (EDS) more in men, more in diastolic failure, and CPAP helps  Mechanisms: HBP worsens systole, hypoxemia worsens diastole. BMI correlates with CHF. LVH may result from OSA independently of HBP.  Hypoxemia & RV afterload  Risk of myocardial infarction  Response to therapy with CPAP, up to 9-12% increase in EF in 3 mos, lowers HR, BP possibly mortality reduction

 Effects of sleep  Mechanical effects

 Autonomic effects  Oxidative, inflammatory, and vascular endothelial

effects  Arrhythmogenic effects  Treatment effects  Chronopharmacology  Reference: OSA and Heart Failure, Pathophysiologic and Therapeutic implications. Kasai and Bradley, JACC Jan,2011, State of the Art Paper.

 62% of TIA patients have AHI > 10/hr  Of 132 stroke patients in rehab, 53 had OSA, CSA or

mixed apenas  Compliance on CPAP after CVA is 15-70%  Severity of OSA correlates with risk of CVA, and

oximetry results after CVA correlate with mortality  Mechanisms: Oxidative stress, hypoxemia, cytokines, A Fib, HBP

 Nocturnal arrhythmias occur in 50% of OSA

pts: NSVT, sinus arrest, second degree heart block, PVC’s, 2-4 fold increase in severe OSA patients.  PVC’s seen in 66% of OSA pts.  VTach seen in sats < 60%  Bradycardia- due to dive reflex after prolonged apnea, REM sleep, hypoxemia. CPAP reverses it.

 59% of pacemaker pts have OSA  OSA seen in 68% of pts with AV block  Mechanisms: Desaturation, dive reflex, REM

sleep, sympathetic stimulation, organic heart disease,  58% reduction with CPAP therapy

Atrial Fibrillation  Obesity and hypoxemia are independent predictors of 

 



A Fib in pts < 65. 82% recurrence of Afib of OSA untreated after cardioversion 50% of pts presenting for cardioversion have OSA (30% in general cardiology population) A Fib role in CVA in OSA pts undetermined Mechanisms: LA stretch more common in OSA, recurrent hypoxemia, intermittent wide catediolamine swings, arousal related startle, especially in REM.Sats dramatically low,

 CAD twice as likely to occur in OSA pts. Usually NOT

Sleepy!  Mechanism: intermittent hypoxemia, acidosis, BP rise, sympathetic vasoconstriction, changes in transmural and transthoracic pressures, all seen in OSA. (Chronically, endothelial dysfunction and inflammation)

 Coronary calcium score correlates with OSA  SDB pts with CAD have more MI’s, CVA’s, and

mortality is higher.  In sudden cardiac death, OSA pts die 10 PM - 6 AM,

and non OSA die 6 AM – 11 AM  CPAP therapy reduces CV events, to same as simple snorers

 EDS common symptom in CRD. OSA 40-60%  Obstructive and Central apneas  Mechanism:  Chronic BP elevations

 Sympathetic nerve discharge  Glomerular hyperfiltration  Periodic limb movement are associated with

premature mortality  Uremia may destablilze central ventilatory control and cause airway edema

 17% of pts with AHI>20 had PAP > 20 most being obese with hypoxemia, hypercapneic  Mechanisms:  Hypoxemia and Acute increase in pressure

 CO & wedge usually normal  Contributors: obesity, hypovent syndrome and

COPD  Marked intrathoracic negative pressure during apnea brings venous return to right heart and pulmonary circuit  CPAP helps lower pressures, by echo

 PFO in 25% of

population  TEE discovers 69% of OSA pts have PFO  Platypnea – orthodeoxia syndrome, migraine with aura, decompression illness and now OSA.

Pathophysiology  Hypoxia during valsalva maneuvers, seen in 1/3 of pts

with PFO and OSA  PFO closure  Neurohumoral factors  Microembolic signals detected during nocturnal apnea is positively correlated with number detected during valsalva in wakefulness, and arterial hypoxemia leads to pulmonary vasoconstriction and hypertension  Closure of PFO in OSA pts needs further investigation and documentation

 Sleep attacks vs. syncope  Central Sleep Apnea

 Cheyne Stokes Breathing  Diabetes (Leptin and weight)

 Pregnancy, and women in general  Mortality  Future research opportunities  “In patients with CAD, if there is even  The slightest suspicion of OSA, perform a PSG.”

A Word About CPAP

CPAP Masks

Positive Airway Pressure

Positive Airway Pressure

A Word About Home Sleep Testing

QUESTION? According to an ACC survey of Cardiologists, the most common barrier to referrals to a sleep center is ? 1) Time needed to take a sleep history 2) Lack of Confidence in accuracy of diagnosis of sleep disorders 3) Concerns over managing Sleep patients 4) Lack of satisfaction over Sleep Apnea therapy options

Barriers To Referring Patients To Sleep Centers • Cardiologists indicate a lack of satisfaction with the effectiveness of sleep apnea therapy as their primary barrier for referring patients to sleep centers. The next barrier was the cost of a sleep study to the patient followed by concerns over managing CPAP therapy. • Only 1 out of 10 (13%) report no barriers to making a sleep center referral. Satisfaction With Sleep Apnea Therapy Cost Of Sleep Study For Patient Concerns Over Managing CPAP Therapy Satisfaction With Sleep Lab Services Patient Refusal/Compliance Time To Discuss Sleep Issues With Patients Discerning Sleep Issues Confidence/Accuracy In Diagnosis Other No Barriers

47% 29% 24% 16% 14% 13% 13% 11% 5% 13%

Q: What are the primary barriers to referring patients to sleep centers for the diagnosis of sleep disordered breathing? (n=76)

Key Findings  Cardiologists tend to believe that a much higher percentage of their 

   

patients suffer from SDB than are diagnosed with it and definitely more than are being currently treated for it. 8 out of 10 cardiologists believe that more than 20% of their patients with heart failure or atrial fibrillation also have sleep disordered breathing or obstructive sleep apnea. 3 out 4 cardiologists are incorporating an assessment of sleep disordered breathing during either the initial patient work up or follow-up visits. 2 out of 3 cardiologists were not aware of the change by Medicare and other payers regarding polysomnography in order to diagnose and then initiate sleep therapy. If a simple home diagnostic test was offered to their practice, more than 2 out of 3 cardiologists indicate that they would likely increase the number of patients tested for sleep apnea per month. The large majority of cardiologists still consider referring patients to sleep centers/labs for a polysomnography test as their top diagnosis model followed by referral to a pulmonologist.

Additional data

SDB Externally • Choking arousals • Fragmented sleep • Nocturia • Unrefreshed on wakening • Morning headaches • Impaired concentration • Daytime sleepiness

Internally • Hypoxemia • Hypercapnia • Sympathetic activation • Endothelial dysfunction • Metabolic dysregulation • Hypertension • Arrhythmias • Myocardial infarction • Stroke

Metabolic Syndrome  Sleep-disordered

breathing is at the center of Metabolic Syndrome  Treating SDB

improves all major co-morbidities

Obesity Trends* Among U.S. Adults (*BMI 30, or about 30 lbs. overweight for 5’4” person)

1998

1990

2008

Journal of Sleep: CDC Behavior Risk Factor Surveillance Survey (BRFSS)

No Data