Weber T, Tschernich H, Sitzwohl C, Ullrich R, Germann P, Zimpfer M, Sladen R N, Huemer G
Department of Anesthesiology and General Intensive Care, University of Vienna, Austria.
Am J Respir Crit Care Med. 2000 Oct;162(4 Pt 1):1361-5. doi: 10.1164/ajrccm.162.4.9808092.
In patients with acute respiratory distress syndrome (ARDS), permissive hypercapnia is a strategy to decrease airway pressures to prevent ventilator-induced lung damage by lowering tidal volumes and tolerating higher arterial carbon dioxide tension. However, in experimental studies hypercapnia impairs myocardial contractility and hemodynamic function. We investigated the effect of short-term permissive hypercapnia on myocardial contractility and hemodynamics in patients with ARDS. We hypothesized that the administration of tromethamine (THAM), a buffer which does not increase carbon dioxide production, would modify these changes. In 12 patients with ARDS, permissive hypercapnia was implemented for 2 h with a target Pa(CO(2))of 80 mm Hg. Patients were randomized to have respiratory acidosis corrected by THAM (pH-corrected group), or not corrected (pH-uncorrected group). Hemodynamic responses were measured, and transesophageal echocardiography (TEE) was used to determine myocardial contractility. Permissive hypercapnia resulted in significant decreases in systemic vascular resistance (SVR) and increases in cardiac output (Q). Myocardial contractility decreased in both groups but significantly less in the pH-corrected group (approximately 10%) than in the pH-uncorrected group (approximately 18%, p < 0.05). Mean arterial pressure decreased and mean pulmonary arterial pressure increased significantly only in the pH-uncorrected group. All values returned to baseline conditions 1 h after permissive hypercapnia was terminated. Our study demonstrates a reversible depression of myocardial contractility and hemodynamic alterations during rapid permissive hypercapnia which were attenuated by buffering with THAM. This may have applicability to the clinical strategy of permissive hypercapnia and allow the benefit of decreased airway pressures to be realized while minimizing the adverse hemodynamic effects of hypercapnic acidosis.
在急性呼吸窘迫综合征（ARDS）患者中，允许性高碳酸血症是一种通过降低潮气量和耐受更高的动脉血二氧化碳分压来降低气道压力以预防呼吸机诱发肺损伤的策略。然而，在实验研究中，高碳酸血症会损害心肌收缩力和血流动力学功能。我们研究了短期允许性高碳酸血症对ARDS患者心肌收缩力和血流动力学的影响。我们假设给予不增加二氧化碳生成的缓冲剂三羟甲基氨基甲烷（THAM）会改变这些变化。在12例ARDS患者中，实施允许性高碳酸血症2小时，目标动脉血二氧化碳分压（Pa(CO₂)）为80 mmHg。患者被随机分为用THAM纠正呼吸性酸中毒的组（pH纠正组）和不纠正的组（pH未纠正组）。测量血流动力学反应，并使用经食管超声心动图（TEE）来确定心肌收缩力。允许性高碳酸血症导致体循环血管阻力（SVR）显著降低和心输出量（Q）增加。两组心肌收缩力均下降，但pH纠正组（约10%）比pH未纠正组（约18%，p < 0.05）下降明显更少。仅在pH未纠正组平均动脉压下降且平均肺动脉压显著升高。允许性高碳酸血症终止1小时后所有值均恢复至基线状态。我们的研究表明，快速允许性高碳酸血症期间心肌收缩力的可逆性降低和血流动力学改变可通过THAM缓冲而减轻。这可能适用于允许性高碳酸血症的临床策略，并在最小化高碳酸血症酸中毒的不良血流动力学影响的同时实现降低气道压力的益处。
