(Circulation. 1999;99:2709-2712.)
© 1999 American Heart Association, Inc.
Correspondence |
Clinical Significance of Arterial Blood Gas Analysis for Detection and/or Treatment of Central Sleep Apnea in Patients With Heart Failure
Department of Geriatric Medicine, Tokyo University Hospital, Tokyo, Japan
To the Editor:
In a recent issue of Circulation, Javaheri et al1 demonstrated that sleep-disordered breathing (SDB), including central sleep apnea (CSA) and periodic breathing (eg, Cheyne-Strokes respiration), is extremely common in patients with stable heart failure and that atrial fibrillation, ventricular arrhythmia, and low left ventricular function are associated with sleep apnea in these patients. Because the reversal of SDB by nasal continuous positive pressures and oxygen may lead to improvements in markers of cardiovascular outcome in selected patients with congestive heart failure (CHF), all cardiologists should pay attention to the recent study. However, the mechanisms of SDB in patients with CHF were not extensively discussed in the article. The same authors recently proposed that low PaCO2 resulted in ventilatory instability and central apnea during sleep.2 In the previous study, the values of PaCO2 were 37±5 and 39±4 mm Hg in patients with SDB and those without SDB, respectively. Although the differences in resting PaCO2 in arterial blood gas between awake patients with SDB and those without SDB were very small, experimental human study suggested that central apnea could be induced by lowering PaCO2 1 to 3 mm Hg below resting PaCO2 while patients were awake.3 In addition, instability in the ventilatory control system might be involved in periodic breathing.4 The higher prevalence of CSA in patients with SDB is at least in part explained by ventilatory instability as indicated by low PaCO2. Wilcox and coworkers5 also revealed that CHF patients with CSA had decreased awake end-tidal CO2 tension (4.1±0.5 kPa), increased ventilatory response to CO2, and eucapnic hypoxic responses in the normal range, but that CHF patients with obstructive sleep apnea had a normal awake end-tidal CO2 tension and normal ventilatory response to CO2. These data indicated that ventilatory instability and augmented chemosensitivity to hypercapnia were important factors in the pathophysiology of CSA in patients with CHF. In addition, it is known that oxygen effectively reduces CSA but not obstructive sleep apnea in patients with CHF. This suggests that oxygen supplementation therapy may be beneficial for both cardiac function and SDB in patients with CHF. Considered together, the assessment of arterial blood gases is particularly important for both detection and treatment of CSA in patients with CHF.
References
1.
Javaheri S, Parker TJ, Liming JD, Corbett WS,
Nishiyama H, Wexler L, Roselle GA. Sleep apnea in 81 ambulatory male
patients with stable heart failure: types and their prevalences,
consequences, and presentations. Circulation. 1998;97:2154–2159.
2.
Javaheri S, Corbett WS. Association of low
PaCO2 with central apnea and
ventricular arrhythmias in ambulatory patients with
stable heart failure. Ann Intern Med. 1998;128:204–207.
3.
Skatrud JB, Dempsey JA. Interaction of sleep state and
chemical stimuli in sustaining rhythmic ventilation. J Appl
Physiol. 1983;55:813–822.
4. Cherniack NS, Longobardo GS. Cheyne-Stokes breathing: an instability in physiologic control. N Engl J Med. 1973;288:952–957.
5. Wilcox I, NcNamara SG, Dodd MJ, Sullivan CE. Ventilatory control in patients with sleep apnea and left ventricular dysfunction: comparison of obstructive and central sleep apnea. Eur Respir J. 1998;11:7–13.
Response
Sleep Disorders Laboratory, Department of Veterans Affairs Medical Center, Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio
We thank Drs Teramoto and Ouchi for their interest in and comments on our work.1 2 We echo their comment, "all cardiologists should pay attention to the recent study." This was the reason for publication of our research work in Circulation.1
Due to the length of the article,1 we did not discuss the mechanisms or treatment of sleep apnea in heart failure and systolic dysfunction, but we have covered these issues elsewhere.2 3 4
Regarding PaCO2, however, the values quoted (Table 2 of Reference 1) included heart failure patients without (PaCO2=39±4 mm Hg) or with (PaCO2=37±5 mm Hg) sleep apnea. Although these values were significantly different, the group with sleep apnea included both central (39% of all heart failure patients) and obstructive (11% of all heart failure patients) sleep apnea.
Regarding central sleep apnea, our previous data2 in a relatively large number (n=59) of patients with heart failure and systolic dysfunction showed that 14 of 18 hypocapnic patients had central sleep apnea. However, 16 of 41 eucapnic patients also had central sleep apnea. In other words, out of 30 heart failure patients who had central sleep apnea, 14 (47%) were hypocapnic. Therefore, an awake low PaCO2 is not a prerequisite for development of central sleep apnea in patients with heart failure, although it highly predicts it. Meanwhile, there are other markers associated with central sleep apnea in heart failure; these include presence of atrioventricular arrhythmias and a very low left ventricular ejection fraction,1 which should serve as clues to the potential presence of central sleep apnea.
With regard to obstructive sleep apnea in heart failure, patients are commonly obese and have a history of loud habitual snoring,1 features similar to those patients with obstructive sleep apnea-hypopnea syndrome without heart failure and systolic dysfunction.
The various therapeutic approaches have also been briefly reviewed elsewhere.3 However, longitudinal studies are necessary to determine whether the natural history of heart failure (particularly the mortality rate, which remains high in spite of the use of ACE inhibitors and carvedilol) is changed by administration of O2, continuous positive airway pressure, or medications. Meanwhile, until such data are available, we recommend that the first therapeutic step is optimization of left ventricular systolic function and treatment of subtle volume overload and pulmonary congestion. If sleep apnea persists, there are several therapeutic options available.3 5 However, careful follow-up is necessary.
References
1. Javaheri S, Parker TJ, Liming JD, Corbett WD, Nishiyama H, Wexler L, Roselle GA. Sleep apnea in 81 ambulatory male patients with stable heart failure: types and their prevalences, consequences, and presentations. Circulation. 1998;97:2154–2159.
2. Javaheri S, Corbett WS. Association of low PaCO2 with central sleep apnea and ventricular arrhythmias in ambulatory patients with stable heart failure. Ann Intern Med. 1998;128:204–207.
3. Javaheri S. Central sleep apnea-hypopnea syndrome in heart failure: prevalence, impact, and treatment. Sleep. 1996;19:S229–S231.[Medline] [Order article via Infotrieve]
4.
Javaheri S, Parker TJ, Wexler L, Liming JD, Lindower
P, Roselle GA. Effect of theophylline on sleep-disordered breathing in
heart failure. N Engl J Med. 1996;335:562–567.
5. Naughton MT, Liu PP, Benard DC, Goldstein RS, Bradley TD. Treatment of congestive heart failure and Cheyne-Stokes respiration during sleep by continuous positive airway pressure. Am J Respir Crit Care Med. 1995;151:92–97.[Abstract]
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