(Chest. 2000;117:271S-273S.)
© 2000
American College of Chest Physicians
Chronic Alveolar Hypoventilation Helps To Maintain the Inspiratory Muscle Effort of COPD Patients Within Sustainable Limits*
Paul Bégin, MD, PhD and
Alejandro Grassino, MD
*
From the Complexe hospitalier de la Sagamie (Dr. Bégin) and Hôpital Notre-Dame du Centre hospitalier de l’Université de Montréal (Drs. Bégin and Grassino), Canada.
Correspondence to: Paul Bégin, MD, Complexe hospitalier de la Sagamie, 305, Rue St-Vallier, Quebec PQ, Canada G7H 5H6
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Introduction
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Abbreviations: Pi = inspiratory pressure;
PImax = maximal inspiratory pressure;
TI/TT = inspiratory duty cycle; TTi =
tension-time index of the inspiratory muscles;
A = alveolar ventilation;
CO2 = carbon dioxide output;
VD/VT = physiologic dead space ventilation;
Z = mechanical impedance
When
the load imposed on the inspiratory muscles is excessive relative to the
neuromuscular capacity, patients need mechanical
ventilation.1
Patients breathing with a tension-time index
of the inspiratory muscles (TTi) above a threshold value between 0.12
and 0.15 have been found to be difficult to wean from the
ventilator.2
The resting TTi of stable patients with COPD
and chronic hypercapnia have also been shown to be
increased.3
4
However, the mechanisms leading to chronic
alveolar hypoventilation in COPD are still debated.4
5
We
reasoned that patients in steady state must maintain their inspiratory
effort within sustainable limits and that alveolar hypoventilation
might serve that purpose. The concept of a critical TTi value provides
a framework to validate our hypothesis.
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Theoretical Considerations
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To assess the relationship between inspiratory muscle loading and
PaCO2, we developed the ventilation
equation as to express minute ventilation using its inspiratory
mechanical determinants6
:
where CO2 = carbon
dioxide output, Z = mechanical impedance (mean inspiratory pressure
[Pi]/mean inspiratory flow),
VD/VT = physiologic dead space ventilation;
K = 0.863 mm Hg; and TI/TT = inspiratory
duty cycle. The equation predicts that
PaCO2 is directly related to a
combination of metabolic and mechanical loads and, for any given load,
is inversely related to the inspiratory muscle effort. To reflect
physiologic constraints, one may divide the mechanical load and the
inspiratory effort in the above equation by maximal inspiratory
pressure (PImax). The
Z/PImax x (1 - VD/VT)
expression can then be simplified into the TTi/alveolar ventilation
(A) ratio, and the
TI/TT [times] Pi/PImax
into TTi.
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Materials and Methods
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We reexamined these relationships by comparing gas exchange and
pulmonary mechanics in a previously reported3
population
of clinically stable COPD patients with a wide range of airway
obstruction (FEV1/FVC < 70%). From 304
available charts, we selected patients with body mass index < 35
kg/m2 whose respiratory acidosis
(H+ = 40.7 ± 3.1 nmol/L,
PaCO2 = 51.8 ± 7.3 mm Hg,
n = 51) or respiratory alkalosis (H+
= 34.8 ± 1.4 nmol/L,
PaCO2 = 32.3 ± 2.0 mm Hg,
n = 12) were compatible with a primary acid-base
disorder,7
8
along with patients with
PaCO2 and H+
values in the normal 35 to 45 range (n = 199). To avoid the effect of
esophageal balloon on breathing, TTi was corrected for the level of
minute ventilation measured during steady-state ventilation.
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Results
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PaCO2 was found to be directly
related to Z (r = 0.55), and even more closely to
Z/(1 - VD/VT) (r = 0.64) and to
the product of this parameter with CO2
(r = 0.65). The TI/Tt x Pi product was also
found to be highly related to Z (r = 0.90), hence to be
directly related to PaCO2
(r = 0.44, p < 0.001). Multiple regression analysis
showed that hypercapnia was associated to a lower inspiratory effort
for a given load in the following equation:
where all are p < 0.001; r = 0.97; Pi is
expressed in centimeters of water, Z is expressed in centimeters of
water per liter per second,
CO2 is expressed in liters per
minute, and PaCO2 is expressed in
millimeters of mercury.
Figure 1
illustrates the relationship between TTi and A in
hypercapnic (black triangles), normocapnic (open circles), and
hypocapnic subjects (open inverse triangles). Hypercapnic subjects are
shown to have the highest TTi values along with the lowest
A values, thus the highest energetic cost of
A. The reverse was found in hypocapnic subjects. All
patients were found to develop a TTi value below or within of the
critical zone described as a determinant of weaning
outcome,2
and far below the 0.27 to 0.30 threshold value
sustained for 1 h by normal subjects during endurance
runs.9
Overall, PaCO2
was found to be closely related to the TTi/A ratio
(r = 0.62).
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Discussion
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Patients with hypercapnia were found to have a TTi value
(mean ± SEM) of 0.071 ± 0.037. In these patients, the equation
allows to estimate the TTi required to achieve normocapnia at
0.092 ± 0.051, assuming constant
CO2 and
TTi/A. However, this calculation most likely
underestimates the inspiratory effort needed to normalize
A, since these patients are expected first to
develop dynamic hyperinflation when increasing
ventilation10
; second, to adopt a rapid and shallow
breathing pattern when approaching the critical TTi
value2
; and third, to increase
CO2 due to increased work of
breathing. Hence, the mechanical and metabolic loads are expected to
increase more than the level of ventilation.
Our results are in keeping with the findings of others, that resting
PaCO2 in COPD is related to
inspiratory work per liter of ventilation11
and to peak
inspiratory flow (reflecting inspiratory load).12
They
also show that the fatigue threshold values of inspiratory muscles are
not reached in stable hypercapnic COPD patients. Hence, the inspiratory
cost of A (TTi/A), rather than
inspiratory muscle fatigue, appears to be a major determinant of
chronic hypercapnia in COPD. The greater the TTi/A
ratio is, the greater the reduction in TTi resulting from alveolar
hypoventilation.
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Conclusion
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Patients with COPD and chronic alveolar hypoventilation need to
develop a higher TTi to fight increased mechanical loads; alveolar
hypoventilation helps to maintain the inspiratory muscle effort within
sustainable limits.
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References
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Zakynthinos, S, Vassilakopoulos, T, Roussos, C (1995) The load on inspiratory muscles in patients with mechanical ventilation. Am J Respir Crit Care Med 152,1034-1040[Abstract]
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Vassilakopoulos, T, Zakynthinos, S, Roussos, C (1998) The tension-time index and the frequency/tidal volume ratio are the major pathophysiologic determinants of weaning failure and success. Am J Respir Crit Care Med 158,378-385[Abstract/Free Full Text]
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Bégin, P, Grassino, A (1991) Inspiratory muscle dysfunction and chronic hypercapnia in chronic obstructive pulmonary disease. Am Rev Respir Dis 143,905-912[ISI][Medline]
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Montes de Oca, M, Celli, BR (1998) Mouth occlusion pressure, CO2 response and hypercapnia in severe chronic obstructive pulmonary disease. Eur Respir J 12,666-671[Abstract]
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Folgering, H, Bégin, P, Grassino, A, et al (1999) CO2-response in chronic obstructive pulmonary disease [letter]. Eur Respir J 13,1211-1214[Medline]
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Grassino, AE, Bégin, P (1996) Role of respiratory muscle dysfunction in ventilatory failure. Derenne, FP Whitelaw, WA Similowski, T eds. Acute respiratory failure in chronic obstructive pulmonary disease ,65-78 Marcel Dekker New York, NY.
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Brackett, NC, Wingo, CF, Muren, O, et al (1969) Acid-base response to chronic hypercapnia in man. N Engl J Med 280,124-130
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Krapf, R, Beeler, I, Hertner, D, et al (1991) Chronic respiratory alkalosis: the effect of sustained hyperventilation on renal regulation of acid-base equilibrium. N Engl J Med 324,1394-1401[Abstract]
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Zocchi, L, Fitting, JW, Majani, V, et al (1993) Effect of pressure and timing of the contraction on human rib cage muscle fatigue. Am Rev Respir Dis 147,857-864[ISI][Medline]
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Pardy, RL, Roussos, C (1983) Endurance of hyperventilation in chronic airflow limitation. Chest 83,744-750[Abstract/Free Full Text]
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Park, SS (1965) Factors responsible for carbon dioxide retention in chronic obstructive pulmonary disease. Am Rev Respir Dis 92,245-254[Medline]
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Molho, M, Shumlimjon, T, Benzaray, S, et al (1993) Importance of inspiratory load in the assessment of severity of airway obstruction and its correlation with CO2 retention in chronic obstructive pulmonary disease. Am Rev Respir Dis 147,45-49[Medline]
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Introduction
Theoretical Considerations
45 mm Hg) are shown in black
triangles, those with hypocapnia (PaCO2 < 35
mm Hg) as open inverse triangles, and those with normocapnia as open
circles. Means ± SEM of each group are shown from the hypocapnic
group in the right lower corner to the hypercapnic group (left upper
bars). The critical zone represent a TTi value very unlikely to be
found in stable COPD patients, similar to that reported by
Vassilakopoulos et al.