Jørgensen L H, Thaulow E, Refsum H E
Department of Clinical Physiology, Ullevål Hospital, Oslo, Norway.
Clin Cardiol. 1997 Sep;20(9):773-7. doi: 10.1002/clc.4960200912.
The mechanisms underlying the excessive ventilatory response to exercise in patients with cardiac failure are still not fully understood.
This study was undertaken to investigate the mechanisms behind exercise hyperpnea in patients with exercise-induced left ventricular dysfunction.
In 18 patients, aged 57-82 years, all with atherosclerotic lumbar aorta aneurysm and pulmonary artery wedge pressure (PAWP) > 25 mmHg during supine exercise, ventilation (V), central hemodynamics, and arterial and venous blood gases were examined during supine rest and exercise, before and during infusion of glyceryl trinitrate (GTN).
Before GTN, exercise PAWP was 32.2 +/- 6.1 mmHg and V/V O2 was 33.8 +/- 7.7 l/l (130% of predicted). With GTN, exercise PAWP was markedly reduced to 15.3 +/- 3.8 mmHg (p < 0.001), whereas V/V O2 was only marginally reduced to 32.3 +/- 3.0 l/l (124% of predicted) (p < 0.05). Exercise physiologic dead space (VD/VT) declined from 0.31 +/- 0.16 to 0.26 +/- 0.17 (p < 0.05), while PaCO2 was reduced from 5.20 +/- 0.31 to 5.10 +/- 0.24 kPa (p < 0.05). PvO2 and cardiac output (CO), however, were unchanged below normal.
The data show that exercise-induced hyperpnea was not substantially reduced by rapid normalization of PAWP and could not be related to preservation of normal PaCO2 in the presence of high VD/VT. The persistence of exercise hyperpnea and reduced PvO2 after GTN is consistent with augmented ventilatory stimuli from hypoxia-induced metabolic abnormalities in the skeletal muscles, or/and persistently reduced CO, due to changes in the integrated superior command of ventilation and circulation.
心力衰竭患者运动时过度通气反应的潜在机制仍未完全明确。
本研究旨在探究运动诱发左心室功能障碍患者运动性呼吸急促背后的机制。
对18例年龄在57 - 82岁之间、均患有动脉粥样硬化性腹主动脉瘤且仰卧位运动时肺动脉楔压（PAWP）>25 mmHg的患者，在仰卧位休息及运动期间，于输注硝酸甘油（GTN）之前及期间，检测其通气（V）、中心血流动力学以及动脉和静脉血气。
在GTN治疗前，运动时PAWP为32.2±6.1 mmHg，V/V O₂为33.8±7.7 l/l（预测值的130%）。使用GTN后，运动时PAWP显著降至15.3±3.8 mmHg（p<0.001），而V/V O₂仅略微降至32.3±3.0 l/l（预测值的124%）（p<0.05）。运动时生理无效腔（VD/VT）从0.31±0.16降至0.26±0.17（p<0.05），同时PaCO₂从5.20±0.31降至5.10±0.24 kPa（p<0.05）。然而，PvO₂和心输出量（CO）在低于正常水平时未发生变化。
数据表明，PAWP快速恢复正常并不能显著减轻运动诱发的呼吸急促，且在高VD/VT情况下，运动诱发的呼吸急促与维持正常PaCO₂无关。GTN治疗后运动性呼吸急促持续存在且PvO₂降低，这与骨骼肌中缺氧诱导的代谢异常增强通气刺激，和/或由于通气与循环的整合高级指令变化导致CO持续降低一致。
