(Circulation. 2001;103:916.)
© 2001 American Heart Association, Inc.
Editorial |
From the Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas.
Correspondence to Robert L. Johnson, Jr., MD, Pulmonary and Critical Care Division, Department of Internal Medicine, 5323 Harry Hines Blvd, Dallas, TX 75390-9034. E-mail Robert.Johnson@utsouthwestern.edu
Key Words: Editorials heart failure ventilation
It has become
increasingly apparent that congestive heart failure (CHF) affects not
only the cardiovascular system, but every organ system involved with
oxygen transport, including the respiratory system, skeletal muscles,
and the hormonal and neural feedback control systems for breathing,
cardiac output, blood pressure, blood volume, and distribution of blood
flow. One segment of this transport system cannot be isolated from the
rest. The ventilatory response to exercise in patients with CHF is
augmented despite normal arterial O2 saturation
and a normal or low end-tidal
PCO2.1 2 3 4 5 6
The augmented ventilatory response is measured as a steep slope of the
increase in ventilation with respect to CO2
output
(
E/
CO2)
or as a high
E/
CO2
ratio at peak exercise. The source of this ventilatory augmentation has
been controversial, but its pathophysiological significance is clear. A
high slope at submaximal exercise or a high
E/
CO2
ratio at peak exercise is a powerful index of poor prognosis in
patients with
CHF.4 7 As
indicated by Ponikowski et
al8 in the current issue of
Circulation, this prognostic
power is retained in patients with CHF, even when the maximal
O2 uptake
(
O2
max) is near the normal range.
A high
E/
CO2
ratio has 2 possible sources: (1) increased ventilation, which is
required to overcome a large dead space to maintain a normal arterial
CO2 tension
(PaCO2),
or (2) increased central drive to ventilation, which drives the
PaCO2
below what is normally expected.
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