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Normally during sleep, there is predominance of parasympathetic activity. During Non-
REM sleep, heart rate, Blood Pressure, and Cardiac Output are reduced. During REM
sleep, heart rate, BP and Cardiac Output fluctuate but are still at levels lower than
awake state. During an obstructive event, large intrathoracic pressures are generated
due to breathing efforts against closed glottis; this increases venous return and also
transmural pressure across myocardium is increased causing increased afterload.
There is increased sympathetic activity due to arousal causing an increase in Heart
Rate and Blood Pressure. Reduced oxygen delivery to myocardium due to hypoxia
may cause myocardial ischemia and/or arrhythmia. Hypoxia and Hyercarbia also
cause an increase in sympathetic activity.

Several studies have shown strong association between OSA and Hypertension
independent of age, obesity, or other confounding factors. Sleep Heart Health study
(cross sectional study of 6,132 subjects) revealed that prevalence of HTN increases
with increasing AHI. In another cross sectional study of 1609 subjects (Wisconsin
Sleep Cohort study), an odd ratio of 3.1 noted for prevalence of HTN with AHI >30.
Also, when these subjects were followed up for 4- 8 years, odds ratio for new onset of
HTN was 2.89 with presence of OSA. It is believed that 40% patients with HTN have
OSA and about 30% patients with OSA have HTN. Drug resistant HTN is more
common in patients with OSA. Treatment of OSA in patients with OSA and HTN
improves control of HTN and at times, may allow discontinuation of medications.
Treatment of OSA in patients without HTN may also prevent development of HTN. Joint
National Committee on Treatment of HTN recommended to exclude OSA in patients
with resistant HTN in 1997. In 2003, they identifies OSA as most common identifiable
cause of HTN.

In Sleep Heart Health Study, patients with OSA reported an increase in coronary artery
events (unstable angina, Stable angina, Myocardial infarction). In one study, clinically
significant OSA was noted in 50% patients with coronary artery disease. Patients with
OSA may have nocturnal ST segment changes that correlate with oxygen desaturation
and severity of OSA. Five year outcome in patients with ischemic heart disease is
negatively influenced in those with OSA compared with those without.

OSA has been associated with idiopathic cardiomyopathy and congestive heart failure
(CHF). Sleep Disordered Breathing in patients with CHF can be obstructive (upper
airway collapse, increased soft tissue edema), central (cheyne stokes respiration) or a
combination of both. In Sleep Heart Health Study, odd ratio of having CHF in patients
with AHI>11 is 2.38. OSA is noted in 11—37% patients with CHF. OSA causes Left
Ventricular Hypertrophy and thus is associated with systolic and diastolic dysfunction.
Several studies have indicated that treatment of OSA in patients with CHF is very
beneficial. Patients with Cheyne Stokes Respiration and CHF did well with CPAP
treatment and had improved transplantation free survival as compared to patients who
did not receive CPAP treatment for Cheyne Stokes respiration. Role of OSA in
causing Pulmonary HTN is not clear. Most believe OSA by itself may cause only mild
Pulmonary HTN.

Significant cardiac arrhythmia due to OSA are rare and may occur only in patients with
severe OSA. Most common arrhythmia noted is cyclic variation of Heart Rate (tachy-
brady arrhythmia). They may also show prolonged sinus arrest, Mobitz Type II Block as
well. In patients with underlying ischemic heart disease or CHF, OSA may precipitate
more significant arrhythmias (ventricular tachycardia, ventricular fibrillation, atrial
fibrillation). In patients with recurrent atrial fibrillation after cardioversion, OSA may be
underlying factor and its treatment may allow stabilization of sinus rhythm in this group of
patients.




	EVALUATE FOR POSSIBLE OBSTRUCTIVE SLEEP APNEA ………. Newly diagnosed Hypertension Drug Resistant Hypertension Requiring 2-3 antihypertensives Coronary artery disease syndromes (stable angina, unstable angina, myocardial infarction) Congestive Heart Failure, Idiopathic Cardiomyopathy Diastolic Dysfunction Left Ventricular Hypertrophy Symptomatic and Asymptomatic bradyarrhythmia Tachy-Brady arrhythmia on Holter monitor Recurrent Atrial Fibrillation