Sleep apnea and heart valve problems, Does CPAP reduce cardiovascular risk?

Obstructive sleep apnea (OSA) is a well-established risk factor for various cardiovascular events due to its effects on oxygen levels, sympathetic nervous system activation, and systemic inflammation.

How OSA contributes to cardiovascular complications

  1. Hypertension: OSA leads to repeated episodes of hypoxia (low oxygen levels) and hypercapnia (high COâ‚‚ levels), activating the sympathetic nervous system. This results in increased blood pressure and a higher risk of resistant hypertension, which does not respond well to standard medications.
  2. Coronary Artery Disease (CAD): Chronic intermittent hypoxia promotes oxidative stress and inflammation, leading to endothelial dysfunction. This increases the risk of atherosclerosis and plaque formation, which can result in heart attacks (myocardial infarction).
  3. Arrhythmias (Irregular Heart Rhythms): OSA is strongly linked to atrial fibrillation (AFib) and other arrhythmias. The repetitive oxygen drops and surges in blood pressure trigger autonomic dysfunction, increasing the likelihood of abnormal heart rhythms.
  4. Heart Failure: OSA increases afterload (pressure the heart must pump against) and reduces oxygen supply, causing left ventricular hypertrophy (LVH) and worsening heart failure with reduced ejection fraction (HFrEF) and preserved ejection fraction (HFpEF). It also contributes to pulmonary hypertension, further straining the heart.
  5. Stroke: OSA is an independent risk factor for ischemic and hemorrhagic strokes due to poor cerebral perfusion, increased blood pressure variability, and inflammation. Patients with OSA who suffer a stroke often have worse recovery outcomes.
  6. Sudden Cardiac Death: OSA increases the risk of sudden cardiac death, especially during sleep, due to severe oxygen desaturation, bradyarrhythmias, and ventricular arrhythmias.

How CPAP Therapy Helps

Continuous Positive Airway Pressure (CPAP) therapy significantly reduces cardiovascular risk by:

Sleep apnea and Cardiovascular events

Sleep apnea and Cardiovascular events

Effects of the upper airway obstruction on CVS (Natural History):

  1. Acute: Inspiration against an occluded upper airway→↓ intrathoracic pressure (-60 mmHg) →↑ venous return to Rt ventricle will compress on the left one by shifting the interventricular septum towards the Lt ventricle and decrease the cavity →↓ Lt ventricular end-diastolic volume (by mechanism of interventricular dependence)→↓ Lt ventricular compliance, Lt ventricular filling, Lt ventricular SV [Paradoxical Septal Movement].
  2. Chronic: Due to sympathetic overactivity and intermittent hypoxemia, patients with OSA are at increased risk of adverse clinical outcomes.

Intermittent hypoxia results in the Reoxygenation and Release of free radicals what’s called oxidative stress >> release certain mediators cause systemic inflammation and endothelial dysfunction in:

  • Cerebrovascular system >> stroke.
  • Systemic circulation >> HTN.
  • CVS morbidity >> HF.
  • Coronaries » IHD.

Patients with untreated severe OSA appear to have an increased risk of all-cause mortality compared to individuals without OSA. These can impair myocardial contractility and cause the development and progression of heart failure.

OSA is associated with systemic hypertension and is a recognized cause of resistant hypertension. Positive airway pressure treatment for OSA is associated with modest but significant reductions in blood pressure.

Coronary heart disease, heart failure, strokes, and arrhythmias are more prevalent in patients with OSA than in the normal population. The most common arrythmia associated with apneic episodes is nocturnal bradyarrhythmia’s,

Arrhythmias in OSA

1) Sinus Brady tachyarrhythmia:

The onset of bradycardia coincides with the cessation of respiration (neurally mediated reflex via ↑ vagal afferent activity).

Apnea → Hypoxia in the absence of lung inflation (lung stretch)-→ Bradycardia.

Termination of apnea →↑ sympathetic neural activity + ↓ vagal tone → Sudden Tachycardia.

Cyclical variations in HR on overnight electrocardiographic monitoring should alert the clinician to the possibility of OSA, but its absence does not exclude OSA.

2) Supraventricular Ectopics.

3) Ventricular Ectopics.

4) Atrial Fibrillation.

Existing studies provide sufficient data to establish OSA as a negative predictor of all-cause mortality and recurrent vascular events following stroke. Propensity for night-time cardiac death, which differs from patients without OSA. OSA may be a novel risk factor for nonalcoholic fatty liver diseases.

OSA induces excessive daytime sleepiness, inattention, and fatigue, which impairs daily function, induces, or exacerbates cognitive deficits, and increases the likelihood of errors and accidents. All domains of executive function (a set of cognitive abilities that control and regulate other abilities and behaviors) demonstrated medium to very large impairments in OSA independent of age and disease severity. Executive function demonstrated small to medium improvements with CPAP treatment.

Patients with OSA may be at greater risk for perioperative complications due to intubation difficulty or impaired arousal from sedatives. Diagnosed OSA increases the risk for worse asthma control in older patients. while CPAP therapy may have a greater impact on asthma outcomes. Unrecognized OSA may be a reason for poor asthma control, particularly among older patients.

Obesity Hypoventilation Syndrome (OHVS): Obese with alveolar hypoventilation (hypercapnia and hypoxemia with a normal alveolar-arterial oxygen gradient) and high bicarbonates, pulmonary hypertension and corpulmonale (lower limb edema and congested neck veins). 80% of patients with OHVS also suffer from OSA (Pickwickian syndrome).

Syndrome Z: OSA should always be suspected in patients presenting with the deadly quartet: obesity with dyslipidemia, insulin resistance, and systemic hypertension (Syndrome X). If a patient with syndrome X is found to have OSA (a common association) this is termed syndrome Z.

Diagnostic evaluation

The decision to order a diagnostic sleep study is based on the clinician’s suspicion of disease presence. Diagnostic testing is essential to confirm or exclude OSA. since the clinical features of OSA are nonspecific and the diagnostic accuracy of clinicians’ subjective impression is poor.

Diagnosis

  • Polysomnography (PSG) is the first-line diagnostic study when OSA is suspected.
  • PSG can either be full-night (diagnostic only) or split-night (which includes both diagnosis of SRBDs and pressure titration).
  • Full-night attended, in-laboratory PSG is considered the gold-standard diagnostic test for (SOB).
  • It involves monitoring the patient during a full night’s sleep. Patients who are diagnosed with OSA and choose positive airway pressure therapy are subsequently brought back for another study, during which their positive airway pressure device is titrated (finding the appropriate needed pressure that abolishes the apneas and hypopneas and arousals).

During PSG recording, the following are monitored during sleep:

  • Electro-encephalogram. (used for sleep staging).
  • Electro-cocohale to detect REM stage of step. (used for sleep staging).
  • Electro-myogram.
  • Nasal and oral airflow.
  • Abdominal and chest movements (using belts around the abdomen and thorax).
  • Pulse oximetry: to record oxygen saturation.
  • ECG monitoring.

Management

1. Continuous positive airway pressure (CPAP):

  • CPAP remains the mainstay of therapy for all patients who have OSA.
  • CPAP delivers a fixed pressure throughout inspiration and expiration, providing a pneumatic splint for the airway that prevents its collapse during sleep.
  • It improves daytime sleepiness in patients with OSA.
  • CPAP also reduces blood pressure among hypertensive patients with OSA, reduces cardiovascular risk, improves neurobehavioral performance, and enhances quality of life. CPAP use is also associated with reduced risk of motor vehicle crashes among drivers with OSA.

2. Behavior modification is indicated for most patients who have OSA. This includes:

  • Losing weight (if overweight or obese). Weight loss has been associated with significant reductions in SOB.
  • Changing the sleep position (if OSA is positional).
  • Oral appliances alter the position of the upper airway structures, enlarging airway caliber and/or reducing airway collapsibility during sleep. Oral appliances are a reasonable alternative to CPAP, particularly for mild to moderate OSA.

3. Surgical therapy: Although multiple surgical options are available to correct upper airway abnormalities leading to obstruction during sleep, the success of these treatments is generally less well-established and less effective than PAP therapy. A notable exception is patients whose OSA is due to a surgically correctable obstructing lesion. For such patients, surgical resection of the obstructing lesion is first-line therapy.

4. Hypoglossal nerve stimulation led to significant improvements in objective and subjective measurements of the severity of OSA

4. Central sleep apnea and Cheyne-Stokes breathing (usually seen in patients with heart failure).

5. Sleep hypoventilation syndrome.

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