(Circulation. 2000;102:2214.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Quantitative General Theory for Periodic Breathing in Chronic Heart Failure and its Clinical Implications
From Royal Brompton Hospital, (D.P.F., K.W., L.C.D., A.J.S.C.) and the National Heart and Lung Institute (D.P.F., L.C.D., A.J.S.C., M.P.), London, UK, and Piacenza Hospital, Italy (M.P.).
Correspondence to D.P. Francis, Heart Failure Unit, Royal Brompton Hospital, Sydney St, London SW36NP, UK. E-mail d.francis{at}cheerful.com
Background—In patients with chronic heart failure (CHF), periodic breathing (PB) predicts poor prognosis. Clinical studies have identified numerous risk factors for PB (which also includes Cheyne-Stokes respiration). Computer simulations have shown that oscillations can arise from delayed negative feedback. However, no simple general theory quantitatively explains PB and its mechanisms of treatment using widely-understood clinical concepts. Therefore, we introduce a new approach to the quantitative analysis of the dynamic physiology governing cardiorespiratory stability in CHF.
Methods and Results—An algebraic formula was derived
(presented as a simple 2D plot), enabling prediction from
easily acquired clinical data to determine whether respiration will be
unstable. Clinical validation was performed in 20 patients with CHF (10
with PB and 10 without) and 10 healthy normal subjects. Measurements,
including chemoreflex sensitivity (S) and delay (
), alveolar volume
(VL), and end-tidal CO2 fraction (
),
were applied to the stability formula. The breathing pattern was
correctly predicted in 28 of the 30 subjects. The principal combined
parameter (S)x(/VL) was higher in
patients with PB (14.2±3.0) than in those without PB (3.1±0.5;
P=0.0005) or in normal controls (2.4±0.5;
P=0.0003). This was because of differences in both
chemoreflex sensitivity (1749±235 versus 620±103 and 526±104 L/min
per atm CO2; P=0.0001 and P<0.0001,
respectively) and chemoreflex delay (0.53±0.06 vs 0.40±0.06 and
0.30±0.04 min; P=NS and P=0.02).
Conclusion—This analytical approach identifies the physiological abnormalities that are important in the genesis of PB and explicitly defines the region of predicted instability. The clinical data identify chemoreflex gain and delay time (rather than hyperventilation or hypocapnia) as causes of PB.
Key Words: heart failure • ventilation • physiology
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