Sullivan M J, Higginbotham M B, Cobb F R
Department of Medicine, Duke University Medical Center, Durham, NC 27710.
Circulation. 1988 Mar;77(3):552-9. doi: 10.1161/01.cir.77.3.552.
This study was designed to determine the pathophysiologic basis of increased exercise ventilation in the presence of chronic heart failure. Sixty-four ambulatory patients with chronic heart failure and 38 age-matched normal control subjects performed exercise according to identical staged, symptom-limited bicycle exercise protocols with measurement of hemodynamic, ventilatory, and metabolic responses. Compared with normal subjects, ventilation and the ratio of ventilation to CO2 production (Ve/VCO2), and pulmonary capillary wedge pressure were elevated in patients at rest and during exercise. The ratio of pulmonary dead space to tidal volume (Vd/Vt) also was elevated in the heart failure group at rest and during exercise and was closely related to Ve/VCO2 (all r greater than .72, p less than .001). Rest and exercise arterial PCO2 regulation was normal in patients. Peak exercise Ve/VCO2 did not correlate with pulmonary vascular pressures, but was inversely related to cardiac output (r = -.49, p less than .001). Thus, neurohumoral ventilatory control mechanisms are intact in patients with chronic heart failure and act to maintain normal PaCO2 levels in the face of increased pulmonary dead space. Activation of abnormal reflexes due to hemodynamic derangements during exercise are not important in determining ventilation in the presence of chronic heart failure. The demonstration of a correlation between decreased cardiac output and increased ventilation in the patient group suggests that attenuated pulmonary perfusion may play a role in causing exercise hyperpnea in the presence of chronic heart failure by producing ventilation perfusion abnormalities and thereby increasing physiologic pulmonary dead space.
本研究旨在确定慢性心力衰竭患者运动通气增加的病理生理基础。64例慢性心力衰竭门诊患者和38例年龄匹配的正常对照者，按照相同的分级、症状限制的自行车运动方案进行运动，并测量血流动力学、通气和代谢反应。与正常受试者相比，患者在静息和运动时通气、通气与二氧化碳产生的比值（Ve/VCO2）以及肺毛细血管楔压均升高。心力衰竭组在静息和运动时肺死腔与潮气量的比值（Vd/Vt）也升高，且与Ve/VCO2密切相关（所有r均大于0.72，p小于0.001）。患者静息和运动时动脉血PCO2调节正常。运动峰值时Ve/VCO2与肺血管压力无关，但与心输出量呈负相关（r = -0.49，p小于0.001）。因此，慢性心力衰竭患者的神经体液通气控制机制完好，在肺死腔增加的情况下能维持正常的PaCO2水平。运动时血流动力学紊乱导致的异常反射激活在慢性心力衰竭患者通气的决定中并不重要。患者组中心输出量降低与通气增加之间存在相关性，这表明在慢性心力衰竭患者中，肺灌注减弱可能通过产生通气灌注异常，从而增加生理性肺死腔，在导致运动性呼吸急促方面发挥作用。
