The indications for specific therapy for nocturnal apnea-hypopnea in heart failure depend on the presence or not of hypoxemia and whether the cause is obstructive or central. Phases of periodic breathing occur in normal subjects, especially in the initial phases of sleep; however, they do not cause hypoxemia >2%. Clinically relevant respiratory dysrhythmia is defined as >15 episodes of periodic respiration per hour of sleep with hypoxemia >5%, measured by simple oximeter. Observation suffices to differentiate between obstructive and central apnea.
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Obstructive apnea, typical of the snorer, is respiratory arrest due to airway obstruction following collapse of the tongue and pharyngeal muscles while the respiratory bellows continues to work at ineffective inspiration. Central apnea is the progressive reduction of respiration until apnea when the rib cage falls still; if it occurs when the patient is half awake, he/she will doze off during apnea and awake abruptly during the ensuing hyperpnea. Such respiratory peri-odism is a major risk for drivers of vehicles.
Any patient shown to have central hypoxia-inducing apnea is classified into in a more severe category of heart failure. Oxygen is effective in the short and long term in reducing nocturnal apnea-hypopnea and is thus the first-line therapy. An alternative is continuous positive airway pressure (CPAP), in which positive pressure is applied via nasal mask or skullcap starting at 5 cm H,0 and increasing by 1 cm H20 every 15 minutes until periodic respiration disappears or the patient awakes.
Positive pressure is then reintroduced after the patient falls asleep. Applied pressures range from 5 to 12 cm H20, with results that are inconsistent but often encouraging. Respiratory periodism, waking, and hypoxemia decrease significantly in 40% to 55% of patients.
Nocturnal cardiac arrhythmia also decreases in CPAP responders vs nonresponders. However, no demographic, clinical, or instrumental feature predicts response. CPAP increases intrathoracic pressure, and decreases respiratory muscle load and left ventricular afterload; it also causes sympathetic activation, probably because of the unloading effect on aortic or cardiopulmonary baroreceptors.
It is also true that in heart failure patients with elevated left ventricular filling pressures CPAP is not associated with hypotension or decreased cardiac output. On the other hand, decreased mitral insufficiency and atrial natriuretic hormone levels, an increased ejection fraction, inhibition of cardiac sympathetic activity, a decreased heart rate, and increased RR variability (probably due to increased parasympathetic tone secondary to pulmonary receptor activation by lung insufflation) have all been documented.
CPAP may thus be effective in under half the patients with respiratory periodism. It does not help patients with non-pathologic respiratory dysrhythmia, and tends to be of greatest benefit in those with moderate rather than severe disease.
Its impact on long-term outcome remains unknown, although a recent randomized controlled study observed significant reductions in mortality and the need for transplantation. The Canadian Positive Airway Pressure (CANPAP) trial is an ongoing multicenter, randomized, controlled clinical trial to test the hypothesis that CPAP therapy for Cheyne-Stokes respiration-central sleep apnea reduces the combined rate of all-cause mortality and cardiac transplantation in heart failure. Secondary outcomes include the severity of central sleep apnea, left ventricular volumes and function, submaximal exercise capacity, quality of life, and hospital admissions.
Keywords: management; periodic breathing; continuous positive airway pressure (CPAP); apnea.