Rationale: Patients with cancer commonly experience dyspnea originating from ventilatory, circulatory and musculoskeletal sources, and dyspnea is best determined by cardiopulmonary exercise testing (CPET). Objectives:...Rationale: Patients with cancer commonly experience dyspnea originating from ventilatory, circulatory and musculoskeletal sources, and dyspnea is best determined by cardiopulmonary exercise testing (CPET). Objectives: In this retrospective pilot study, we evaluated patients with hematologic and solid malignancies by CPET to determine the primary source of their dyspnea. Methods: Subjects were exercised on a cycle ergometer with increasing workloads. Minute ventilation, heart rate, breathing reserve, oxygen uptake (V’O<sub>2</sub>), O<sub>2</sub>-pulse, ventilatory equivalents for carbon dioxide and oxygen (V’<sub>E</sub>/V’CO<sub>2</sub> and V’<sub>E</sub>/V’O<sub>2</sub>, respectively) were measured at baseline and peak exercise. The slope and intercept for V’<sub>E</sub>/V’CO<sub>2</sub> was computed for all subjects. Peak V’O<sub>2</sub> 4% predicted indicated a circulatory or ventilatory limitation. Results: Complete clinical and physiological data were available for 36 patients (M/F 20/16);32 (89%) exhibited ventilatory or circulatory limitation as shown by a reduced peak V’O<sub>2</sub> and 10 subjects with normal physiologic data. The largest cohort comprised the pulmonary vascular group (n = 18) whose mean ± SD peak V’O<sub>2</sub> was 61% ± 17% predicted. There were close associations between V’O<sub>2</sub> and spirometric values. Peak V’<sub>E</sub>/V’O<sub>2</sub> and V’<sub>E</sub>/V’CO<sub>2</sub> were highest in the circulatory and ventilatory cohorts, consistent with increase in dead space breathing. The intercept of the V’<sub>E</sub>-V’CO<sub>2</sub> relationship was lowest in patients with cardiovascular impairment. Conclusion: Dyspneic patients with malignancies exhibit dead space breathing, many exhibiting a circulatory source for exercise limitation with a prominent pulmonary vascular component. Potential factors include effects of chemo- and radiation therapy on cardiac function and pulmonary vascular endothelium.展开更多
文摘Rationale: Patients with cancer commonly experience dyspnea originating from ventilatory, circulatory and musculoskeletal sources, and dyspnea is best determined by cardiopulmonary exercise testing (CPET). Objectives: In this retrospective pilot study, we evaluated patients with hematologic and solid malignancies by CPET to determine the primary source of their dyspnea. Methods: Subjects were exercised on a cycle ergometer with increasing workloads. Minute ventilation, heart rate, breathing reserve, oxygen uptake (V’O<sub>2</sub>), O<sub>2</sub>-pulse, ventilatory equivalents for carbon dioxide and oxygen (V’<sub>E</sub>/V’CO<sub>2</sub> and V’<sub>E</sub>/V’O<sub>2</sub>, respectively) were measured at baseline and peak exercise. The slope and intercept for V’<sub>E</sub>/V’CO<sub>2</sub> was computed for all subjects. Peak V’O<sub>2</sub> 4% predicted indicated a circulatory or ventilatory limitation. Results: Complete clinical and physiological data were available for 36 patients (M/F 20/16);32 (89%) exhibited ventilatory or circulatory limitation as shown by a reduced peak V’O<sub>2</sub> and 10 subjects with normal physiologic data. The largest cohort comprised the pulmonary vascular group (n = 18) whose mean ± SD peak V’O<sub>2</sub> was 61% ± 17% predicted. There were close associations between V’O<sub>2</sub> and spirometric values. Peak V’<sub>E</sub>/V’O<sub>2</sub> and V’<sub>E</sub>/V’CO<sub>2</sub> were highest in the circulatory and ventilatory cohorts, consistent with increase in dead space breathing. The intercept of the V’<sub>E</sub>-V’CO<sub>2</sub> relationship was lowest in patients with cardiovascular impairment. Conclusion: Dyspneic patients with malignancies exhibit dead space breathing, many exhibiting a circulatory source for exercise limitation with a prominent pulmonary vascular component. Potential factors include effects of chemo- and radiation therapy on cardiac function and pulmonary vascular endothelium.
