Gas Exchange Efficiency in Congestive Heart Failure
2000; Lippincott Williams & Wilkins; Volume: 101; Issue: 24 Linguagem: Inglês
10.1161/01.cir.101.24.2774
ISSN1524-4539
Autores Tópico(s)Cardiovascular Function and Risk Factors
ResumoHomeCirculationVol. 101, No. 24Gas Exchange Efficiency in Congestive Heart Failure Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBGas Exchange Efficiency in Congestive Heart Failure Robert L. JohnsonJr Robert L. JohnsonJrRobert L. JohnsonJr From the Division of Pulmonary and Critical Care, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Tex. Originally published20 Jun 2000https://doi.org/10.1161/01.CIR.101.24.2774Circulation. 2000;101:2774–2776The lungs and heart are irrevocably linked in their oxygen and CO2 transport functions. Functional impairment of the lungs often affects heart function, and functional impairment of the heart often affects lung function. In patients with chronic congestive heart failure (CHF), exertional dyspnea is a common symptom, and ventilatory effort is increased at a given exercise workload despite normal arterial blood gases. In this issue of Circulation, the increased exercise ventilation in CHF is reported to contain prognostic information that extends beyond that provided by maximal oxygen uptake (V̇o2max), left ventricular ejection fraction, or the NYHA functional classification.1 Their data indicate that the steepness with which ventilation increases relative to CO2 production during incremental exercise, either alone or in combination with V̇o2max, left ventricular ejection fraction, and NYHA classification, can be a sensitive tool for predicting event-free survival of patients with CHF. Such a tool can be important for evaluating the need for heart transplantation or for following the efficacy of therapeutic measures; it can be evaluated at submaximal work loads and is easier to measure than V̇o2max.The high ventilation (V̇e) with respect to CO2 production (V̇co2) in CHF is not a new observation,23456 but its potential usefulness as a prognostic tool to evaluate the severity of CHF is relatively new. Perhaps even more important, however, is what the studies of Kleber et al,1 using this tool, tell us about impaired gas exchange in CHF and its relationship to impaired gas exchange in lung disease.Because the high level of ventilatory drive in heart failure can predict survival, it must contain important information on how left ventricular dysfunction affects either the lung or ventilatory control. The first thing that we need to examine, then, is what basic information is contained in the slope of the relationship between ventilation (V̇e) and CO2 production (V̇co2). The modified alveolar equation7 concisely describes the determinants of the steepness with which V̇e rises with respect to V̇co2: The relationship between V̇e and V̇co2 by Equation 1 is linear over a wide range, and its slope is determined by just 2 factors: (1) behavior of arterial CO2 tension during exercise and (2) the Vd/Vt ratio. If Paco2 is driven down by a high ventilatory drive from peripheral chemoreceptors or by ergoreceptors in skeletal muscle, the slope of the V̇e/V̇co2 relationship will increase, or if Vd/Vt is high, the V̇e/V̇co2 slope will increase. Increased chemoreceptor gain is often seen in severe CHF,8 eg, in patients with Cheyne-Stokes breathing, but increased chemoreceptor gain alone will not drive the Paco2 down unless the set point about which Paco2 is controlled is depressed or unless hypoxic drive or ergoreceptor drive is high. Most studies suggest that blood gases are normal in patients with CHF4 and that Paco2 either stays the same or declines modestly from rest to peak exercise, no differently than in normal controls. There are 2 potential sources for a high Vd/Vt ratio: (1) a low tidal volume (Vt) with respect to a normal anatomic dead space or (2) an abnormally high physiological dead space. Patients with CHF often have a reduced tidal volume at heavy exercise, which would increase the Vd/Vt ratio; however, it has been estimated that only ≈33% of the increased dead space ventilation in CHF can be explained by a low Vt.25Current information suggests that the major source for an abnormally steep V̇e/V̇co2 slope in CHF is increased nonuniformity of ventilation-perfusion ratios (V̇/Q̇), causing inefficient gas exchange. However, a word of caution is still necessary. The above conclusion is based on indirect evidence. No direct comparisons have been made of Paco2 and dead space ventilation in CHF patients with and without a high V̇e/V̇co2 slope during exercise. Such comparisons are needed.What might be the source of an increased nonuniformity of pulmonary V̇/Q̇ ratios in CHF and why would it provide prognostic information not provided by V̇o2max? Lung volumes and ventilatory function in the CHF patients studied by Kleber et al1 were relatively normal, and arterial blood oxygen saturation at peak exercise was normal, as is generally the case in CHF in the absence of coexisting lung disease. This pattern of a high Vd/Vt ratio with normal arterial blood gases suggests that nonuniformity of V̇/Q̇ ratios in the lung is more likely caused by increased nonuniformity of perfusion than of ventilation. When ventilatory capacity remains normal, inefficient gas exchange caused by abnormal distribution of perfusion usually can be well compensated during exercise by raising ventilation enough to maintain a normal Paco2 and normal arterial blood O2 saturation. This is not true in severe chronic obstructive lung disease, in which not only are ventilation and perfusion poorly matched, but also, compensatory increases in ventilation are restricted by the high resistance to air flow; during exercise, Paco2 rises and arterial blood O2 saturation falls. In the CHF patients studied by Kleber et al1 with high V̇e/V̇co2 slopes, mean total lung capacity (TLC), vital capacity (VC), and lung diffusing capacity (Dlco) were significantly lower than in patients with a normal V̇e/V̇co2 slope, yet arterial O2 saturation remained normal at peak exercise. Dlco is usually reduced in severe CHF9101112 and correlates significantly with V̇o2max. A modest reduction in Dlco may reflect a more severe reduction of true membrane diffusing capacity (Dmco), because the low Dmco in CHF can be counterbalanced by a high pulmonary capillary blood volume (Vc). In patients with severe CHF (NYHA class III) studied by Puri et al,9 Dmco was 35% of control, whereas Dlco was reduced only to 55% of control because of a high Vc (144% of control). The low Dmco implies that oxygen diffusing capacity (Dlo2) is correspondingly reduced, which in turn will reduce the rate of oxygenation of blood perfusing the lungs, and if the cardiac output is high enough, will cause oxygen saturation of blood leaving the lung to fall during exercise. Some of these changes in diffusing capacity and dead space ventilation are reversible with ACE inhibitors and diuretics, reflecting subclinical interstitial pulmonary edema.513 However, persistence of a low Dlco after heart transplantation14 implies additional structural changes in microvasculature, which is confirmed by morphological studies. Muscular arteries and arterioles show medial hypertrophy and intimal and adventitial fibrosis with narrowing vascular lumens.15 Matrix proteins are increased in the alveolar walls, and capillary basement membranes are thickened1617 ; these changes probably begin very early in response to a chronic increase in pulmonary capillary blood pressure from any cause.18In the face of an abnormally high Vd/Vt ratio and a significant reduction of Dlo2 in patients with severe CHF, why is maximal oxygen transport not partially limited by impaired gas exchange associated with a rise in Paco2 and fall in arterial O2 saturation during exercise, as usually occurs in lung disease with similar abnormalities? There are 2 reasons: (1) Maximal ventilatory capacity is well maintained in CHF and can compensate for the high Vd/Vt, bringing the Paco2 down to normal levels at peak exercise and maintaining a normal or high alveolar oxygen tension. (2) Maximal cardiac output (Q̇max) in CHF is reduced more than is the Dlo2; hence, the ratio of Dlo2/Q̇ never falls low enough during exercise to cause a fall of O2 saturation of blood leaving the lung.7It is the low maximal cardiac output and impaired peripheral O2 extraction that primarily impairs oxygen transport in CHF,419 not pulmonary gas exchange; arterial blood gases remain normal. However, the reduced efficiency of gas exchange in CHF reflected by the steep relationship between V̇e and V̇co2 is probably a major source of the exertional dyspnea with normal arterial blood gases.Thus, left ventricular heart failure has important effects on lung function, just as lung disease has important effects on cardiovascular function. The application of a measurement that quantifies efficiency of gas exchange during exercise as an index of the severity of CHF and life expectancy in CHF emphasizes the important functional linkage between the heart and the lungs. The measurement used is simple and can be applied even at low levels of exercise. It must be emphasized, however, that the measurement, ie, the slope of the relationship between V̇e and V̇co2 during exercise, is nonspecific and is frequently abnormally steep in primary lung disease as well as in CHF, although usually associated with abnormal arterial blood gases in lung disease. Hence, the measurement used by Kleber et al1 must be interpreted in context. To emphasize this, a comparison of the primary determinants of impaired gas exchange in CHF, chronic obstructive lung disease, and interstitial lung disease with alveolar capillary block20 are shown in the Table.In the Table, the arrows, pointing either up or down, indicate the change in direction of the key determinants at each step in oxygen transport for each condition. The Table is oversimplified but is conceptually useful. In CHF, the primary impairment of oxygen transport is imposed by a reduced maximal cardiac output (Q̇max), indicated by a boldface arrow pointing down. In patients with chronic obstructive pulmonary disease, primary impairment of oxygen transport is imposed by a reduced maximal ventilation (V̇emax) with inefficient gas exchange, and in patients with interstitial lung disease with alveolar capillary block, the primary impairment is imposed by a reduced Dlo2. In all of these disorders, uneven V̇/Q̇ matching increases the Vd/Vt ratio and impairs the efficiency of CO2 excretion from the lung; if ventilation can be increased enough during increasing exercise to prevent the Paco2 from rising, the V̇e/V̇co2 slope will be steeper than normal in lung disease as well as in CHF, as indicated by the bracketed term in Equation 1. In severe chronic obstructive pulmonary disease, Paco2 will rise as exercise load increases, and the V̇e/V̇co2 slope may become low even though Vd/Vt is high.19 Coexistent lung disease can significantly alter the expected pattern of gas exchange in CHF. Thus, it must be cautioned that if a patient with CHF has significant coexistent lung disease, application of the V̇e/V̇co2 slope to predict survival, as proposed by Kleber et al,1 becomes invalid.In summary, available data suggest that chronic CHF induces structural changes as well as interstitial pulmonary edema in the lungs, which impair the efficiency of gas exchange; the extent of these changes reflects the severity of the CHF and probably its duration. Physiologically, these structural changes are manifested by an increased ratio of dead space to tidal volume (Vd/Vt), which causes an abnormally high ventilation during exercise. They are also usually manifested by a reduction in diffusing capacity of the lung (Dlco), which varies with the severity of CHF. Although the magnitude of these physiological changes in lung function can reflect the severity of CHF and be an important predictor of survival, inefficiency of gas exchange is not the primary cause of impaired exercise capacity. Reduced maximal oxygen transport in CHF is caused by a low maximal cardiac output and perhaps impaired peripheral oxygen extraction; arterial Paco2 and arterial O2 saturation at peak exercise remain normal. Even though arterial blood gases remain normal, inefficient gas exchange can be a major source of exertional hyperpnea and dyspnea. The pattern of abnormal gas exchange during exercise in CHF clearly differs from that in primary lung disease; problems of interpretation arise when CHF and primary pulmonary disease coexist.The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association. Table 1. Determinants of Gas Exchange at Maximal Exercise in Patients With CHF and With Primary Lung Disease Q̇ max V̇ emaxDlo2Vd/VtV̇e/V̇co2 SlopeDlo2/Q̇Paco2Sao2CHF ⬇ N↓↑↑NNNCOPD↓ ⬇ ↓↑V↓V↓IPF↓↓ ⬇ ↑↑ ⬇ ↓ ⬇ COPD indicates chronic obstructive lung disease; IPF, interstitial pulmonary fibrosis; V, variable (can be high, normal, or low); N, normal; ↓, decreased; ↑, increased; and boldface arrow, a primary change. In CHF, the primary determinant of V̇o2max is a low Q̇max; in COPD, the primary determinant is V̇emax; and in IPF with alveolar capillary block, the primary determinant of V̇o2max is a low Dlo2.FootnotesCorrespondence to Robert L. 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June 20, 2000Vol 101, Issue 24 Advertisement Article Information Metrics Copyright © 2000 by American Heart Associationhttps://doi.org/10.1161/01.CIR.101.24.2774PMID: 10859280 Originally publishedJune 20, 2000 KeywordsEditorialsexercisedyspneahyperpneablood gasesPDF download Advertisement
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