A complaint of dyspnea may indicate hyperventilation and altered respiratory rhythm. It was long suspected, and has recently been confirmed, that during sleep over half of heart failure patients display respiratory dysrhythmia, characterized by periodic hypoventilation followed by hyperventilation (hyperpnea). During the hypopneic phases these patients have periods of absent respiratory activity (apnea) of variable duration (Cheyne-Stokes breathing). Patients often refer to the hyperpneic phases that follow apnea and hypopnea as an alarming sensation of lack of air, causing sudden waking with air hunger. Unless elicited by specific direct questioning, the nocturnal dyspnea due to an altered respiratory pattern may be misinterpreted as orthopnea due to nocturnal pulmonary congestion. In fact, however, it may occur in dry uncongested patients with a low cardiac output, in whom it naturally fails to respond to an increase in diuretic dose.
The prevalence of respiratory dysrhythmia in heart failure is uncertain (Table). Most study populations have been small, and all have been marred by selection bias. The Toronto Sleep Research Laboratory has reported the largest study in 450 consecutive heart failure referrals (62%, 34% and 4% in New York Heart Association functional classes II, III, and IV). Sleep apnea, defined as 10 or more hypopneic/apneic episodes/hour of sleep, was present in 71%; it was central in 33%, and peripheral in 38%; when defined as 20 or more hypopneic/apneic episodes/hour, these percentages fell to 25% and 27%. The proportion of sleep apnea was thus high, and comprised a surprisingly high prevalence of the obstructive variant. As is frequently the case, the setting, ie, the sleep laboratory, may have influenced referral patterns. However, in another population with advanced heart failure, 60% to70% exhibited periodic breathing at night and/or during the day; it was also present during exercise and in mild-to-moderate heart failure.
Periodic reduction or absence of respiratory activity is accompanied by a simultaneous reduction in 02 saturation and thus brief, but recurrent, episodes of hypoxia that may total several hours in the course of a day and especially during the night. Hypopnea causes oxygen deficit, while hyperpnea interrupts sleep rhythm and causes sudden and frequent waking with daytime drowsiness and irritability. It is possible, although unproven, that hypoxia due to respiratory dysrhythmia is an independent cause of heart failure progression and a risk factor for sudden death. The incidence of unsustained ventricular tachycardia is high (around 50%) in patients with disturbed sleeping patterns with or without apneic pauses. Hypoxia, as best documented in chronic obstructive airways disease, may cause sudden increases in pulmonary and systemic blood pressure. The hyperpneic phase is associated with increased sympathetic system activity. These factors combine to increase the risk of arrhythmia and/or transient myocardial ischemia. Cerebral hypoxia is an additional impetus to adrenergic activation, and further impairs cognitive and psychologic well-being in subjects weakened by a decreased cerebral blood supply, malnutrition, and the toxicity of renal and hepatic dysfunction. Analyses adjusted for other prognostic determinants show that periodic breathing is a major marker of adverse outcome.
Hypotheses to account for the periodicity of the altered respiratory rhythm include:
Hypersensitivity of central respiratory control centers and peripheral chemoreceptors to small changes in 02 and C02, resulting in input and output amplification of the respiratory response, with a periodicity determined by the periodicity of the stimuli.
Decreased damping capacity by the body due to the decrease in overall 02 and C02 content.
Delayed transmission of information due to the prolonged circulation time between lungs and brain, accentuated, once periodicity is initiated, by the cyclical changes in cardiac output and blood pressure linked to the respiratory phases.
The interest of these interpretations is not only speculative, but will have practical therapeutic implications once they have been resolved.
Javaheri S. Effects of continuous positive airway pressure on sleep apnea and ventricular irritability in patients with heart failure. Circulation. 2000;101:392-397.
Lanfranchi PA, Braghiroli A, Bosimini E, et al. Prognostic value of nocturnal Cheyne-Stokes respiration in chronic heart failure. Circulation. 1999;99:1435-1440.
Lofaso F, Verschueren P, Rande JL, Harf A, Golden berg F. Prevalence of sleep-disordered breathing in patients on a heart transplant waiting list. Chest. 1994;106:1689-1694.
Mortara A, Sleight P, Pinna GD, et al. Abnormal awake respiratory patterns are common in chronic heart failure and may prevent evaluation of autonomic tone by measures of heart rate variability. Circulation. 1997;96:246-252. Naughton MT, Liu PP, Bernard DC, Goldstein RS, Bradley TD. Treatment of congestive heart failure and Cheyne-Stokes respiration during sleep by continuous airway pressure. Am J Crit Care Med. 1995; 151:92-97.
Sin DD, Fitzgerald F, Parker JD, Newton G, Floras JS, Bradley TD. Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure. Am J Respir Care Med. 1999; 160:1101 -1106.
symptom; diagnosis; respiratory dysrhythmia; Cheyne-Stokes respiration; prevalence
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