1. “first episode” vs.
Recurrant
Atrial fibrilation
information sources: Hurst’s THE HEART and UpToDate articles titled:
New Onset Afib and Cardiovascualr Effects of Obstructive Sleep Apnea
6. Treatment of AFib
• No one ideal therapy for all patients
• No therapy, allow A Fib
• Anticoagulation (Coumadin)
• Rate Control (Metoprolol, diltiazem, digoxin) <110 bpm
• Rhythm Control (Amiodarone, Flecainide, Sotolol)
• AV node ablation
• Cardioversion
• Electrical
• Pharmacologic: ex: Irbesartan (ARB), Procainamide, and
other Rhythm control drugs
7. Indications for
EmerGent Cardioversion
• Active ischemia
• Evidence of organ hypoperfusion
• Pulmonary edema
• Atrial Tachycardia (rate >250 bmp)
• Accessory pathway
• <48hours: Heparin
• Unless CHADS2 score 0-1
9. The connection
• Patients with OSA have increased prevalence and
incidence of Systemic HTN
• Apnea Hypopnea Index: >15 events/hour = 3x the HTN
• More severe the OSA= More severe HTN
• Treatment with CPAP can lower Systemic BP
• But not enough to avoid antihypertensive medications
10. Further implications
• Corresponding daytime hypoxia (ex: COPD)
• or excessive daytime sleepiness (with continued
hypoxia/hypercapnea from naps)
• = Worse Cardiovascular effects from OSA
• And possible Pulmonary Hypertension
• Association with Severe OSA and CAD
• Cause or effect??
• Clear studies that OSA worsens CHF
11. OSA And Arrhythmia
• Unclear cause vs. effect relationship
• >30 events/hour, pts had increase in:
• Nocturnal Atrial Fibrilation
• Nonstustained nocturnal VTACH
• In patients with AFIB and Untreated OSA, AFIB is
more likely to reoccur after cardioversion
• 82% vs. 42%
palpitations, a sense of the heart racing, an irregular pulse, fatigue, lightheadedness, increased urination, weakness, and mild shortness of breath. More severe symptoms and signs include dyspnea, angina, hypotension, and presyncope
Patients with obstructive sleep apnea (OSA) experience repetitive episodes of apnea or reduced inspiratory airflow due to upper airway obstruction during sleep. These events are associated with intermittent asphyxia (ie, concomitant hypoxemia and hypercapnia) and usually provoke an arousal from sleep. The arousal is associated with restoration of upper airway patency and ventilation. oscillation of the systemic and pulmonary arterial blood pressures, heart rate, and cardiac function [1]. These hemodynamic changes can be dramatic, even among patients who are normotensive when awake.
Activation of the parasympathetic nervous system may result from hypoventilation, hypoxemia, respiratory acidosis, or vigorous inspiratory effort against a closed airway (Mueller's maneuver).
We believe that all patients who are observed to have nocturnal cardiac arrhythmias (with or without daytime arrhythmias) should undergo diagnostic evaluation for possible OSA. The evaluation should consist of an objective sleep assessment that includes an ECG tracing, so that respiratory events during sleep may be correlated with cardiac arrhythmias. Such an assessment is particularly important for patients who have a chronic pacemaker for any reason, because sleep related breathing disorders are prevalent in this population. CPAP reduces mortality and LV EF% in pts dx with both OSA and CHF
