Exertional hyperpnea in patients with chronic heart failure is a reversible cause of exercise intolerance
- 28 Downloads
Hyperpnea in chronic heart failure occurs even in the absence of considerable impairment of lung function. It is caused by altered respiratory pattern with rapid shallow breathing and ventilation-perfusion mismatch, so far thought to be irreversible.
To test the underlying pathophysiologic disorders and the reversibility of this hyperpnea, i.e., the increased ventilatory response to exercise and its impact on exercise tolerance, 17 patients with chronic heart failure were evaluated before and 4 weeks after adjustment of heart failure therapy with diuretics and ACE inhibitors, and results were compared with normal volunteers.
Ventilatory response to exercise was measured during treadmill exercise by calculation of the slope of the linear relation between minute ventilation (VE) and carbon dioxide output (VCO2) and compared to NYHA class, oxygen consumption at the gas exchange anaerobic threshold (VO2 AT), maximal oxygen uptake (VO2 max) and ventilation of physiological dead space.
VE vs VCO2 slope was related to severity of heart failure (NYHA class). Elevation of VE vs VCO2 slope was strongly correlated to elevated ventilation of physiologic dead space.
Patients were divided into responders (significant decrease of VE vs VCO2 slope of at least 5 1/1 1 CO2) and nonresponders (decrease of VE vs VCO2 slope less than 5 1 or increase). Responders revealed an increase of VO2 AT (7.4±2.6 to 11.7±2.1 ml O2/kg/min; p=0.01) and VO2 max (11.2±2.8 to 17.4±5.3; p=0.005,, while nonresponders showed a non significant decrease of oxygen consumption (VO2 AT 9.6±3.7 to 9.0±3.7; peak VO2 14.6±6.1 to 14.4±6.4), despite adjusted heart failure therapy.
Exercise hyperpnea in heart failure is mainly caused by ventilation of excess physiologic dead space and strongly contributes to severity of symptoms.
Ventilatory response to exercise can be improved by adjustment of heart failure therapy in a considerable proportion of patients. Improvement is associated with an increase in aerobic capacity. Ventilation-perfusion mismatch is a major and modifiable factor determining exercise tolerance in patients with chronic heart failure.
Key wordsVentilatory efficiency ventilation perfusion mismatch dyspnea
Unable to display preview. Download preview PDF.
- 1.Frank NR, Lyons HA, Siebens AA, Nealon TF (1957) Pulmonary compliance in patients with cardiac disease. Am J Med 22: 516–521Google Scholar
- 2.Fink LI, Wilson JR, Ferraro N (1986) Exercise ventilation and pulmonary artery wedge pressure in chronic stable congestive heart failure. Am J Cardiol 57: 249–253Google Scholar
- 3.Janicki JS, Weber KT (1984) Equipment and protocols to evaluate the exercise response. In: Weber KT, Janicki JS (eds) Cardiopulmonary exercise testing. Physiological principles and clinical applications. W.B. SaundersGoogle Scholar
- 4.Wasserman K (1988) New concepts in assessing cardiovascular functions. Circulation, 78: 1060–1070Google Scholar
- 5.Drexler H, Münzel T, Riede U, Just H (1991) Adaptive changes in the periphery and their therapeutic consequences. Am J Cardiol 67: 29C-35CGoogle Scholar
- 6.Sullivan MJ, Higginbotham MB, Cobb FR (1989) Exercise training in patients with chronic heart failure delays ventilatory anaerobic threshold and improves submaximal exercise performance. Circulation 79: 324–329Google Scholar
- 7.Fishman AP, Ledlie JF (1979) Dyspnea. Bull Europ Physiopath Resp 15: 789–804Google Scholar
- 8.Buller NP, Poole-Wilson PA (1990) Mechanism of the increased ventilatory response to exercise in patients with chronic heart failure. Br Heart J 61: 281–283Google Scholar
- 9.Oren A, Wasserman K, Davis JA, Whipp BJ (1981) Effect of CO2 set point on ventilatory response to exercise. J Appl Physiol 51: 185–189Google Scholar
- 10.Ingram RH, McFadden ER, (1976) Respiratory changes during exercise in patients with pulmonary venous hypertension. Progress in Cardiovascular Diseases 19: 109–115Google Scholar
- 11.Sullivan MJ, Higginbottam MB, Cobb FR (1988) Increased exercise ventilation in patients with chronic heart failure: Intact ventilatory control despite hemodynamic and ventilatory abnormalities. Circulation 77: 552–559Google Scholar
- 12.Franciosa JA, Leddy CL, Wilen M, Schwartz DE (1984) Relation between hemodynamic and ventilatory responses in determining exercise capacity in severe congestive heart failure. Am J Cardiol 53: 127–134Google Scholar
- 13.Caiozzo VJ, Davis JA, Berriman DJ, Vandagriff RB, Prietto CA (1987) Effect of high-intensity exercise on the VE-VCO2 relationship. J Appl Physiol 62: 1460–1464Google Scholar
- 14.Metra M, Dei Cas L, Panina G, Visioli O (1992) Exercise hyperventilation in chronic congestive heart failure and its relation to functional capacity and hemodynamics. Am J Cardiol 70: 622–628Google Scholar
- 15.Uren NG, Davies SW, Irwin AG, Jordan SL, Hilson AJW, Agnew JE, Lipkin DP (1991) Regional ventilation-perfusion mismatch and exercise capacity in chronic heart failure. Circulation 84: Suppl II-7 (abstr)Google Scholar
- 16.Yokohama H, Sato H, Ozaki H, Imai K, Li D, Inoue M, Kamada T (1991) Role of reduced ventilatory efficiency in exercise intolerance in chronic heart failure. Circulation 84: Suppl II-73 (abstr)Google Scholar
- 17.Rajfer SI, Nemanich JW, Shurman AJ, Rossen JD (1987) Metabolic responses to exercise in patients with heart failure. Circulation 76: VI-46–53Google Scholar
- 18.Reed JW, Ablett M, Cotes JE (1978) Ventilatory responses to exercise and carbon dioxide in mitral stenosis before and after valvulotomy: causes of tachypnoea. Clinical Science and Molecular Medicine 54: 9–16Google Scholar
- 19.McMichael J (1939) Hyperpnea in heart failure. Clinical Science 4: 19–33Google Scholar
- 20.Theodore J, Robin Ed, Morris AJ, Burke CM, Jamieson SW, van Kessel A, Stinson EB, Shumway NE (1986) Augmented ventilatory response to exercise in pulmonary hypertension. Chest 89: 39–44Google Scholar