Sowton E
Department of Cardiology, Guy's Hospital, London, England.
J Cardiovasc Pharmacol. 1991;17 Suppl 6:S20-3.
Hemodynamic effects during arrhythmias may be caused by underlying pathology (i.e., infarction) as well as disturbance of rate or conduction pattern. In all arrhythmias, compensatory mechanisms tend to restore normal hemodynamics, and with good left ventricular function this can be achieved despite wide disturbance of rhythm. Hemodynamic effects of ectopic beats can result in dramatic fall of stroke volume and reduction in cardiac output, which is greater for ventricular than for atrial ectopics. Prolonged tachycardias are also tolerated up to far higher rates (180/min) if they are atrial, not ventricular, in origin. Mean blood pressure is often maintained even when systolic pressure and cardiac output are reduced. Even in healthy young subjects it is possible for cardiac ischemia to be induced by excessive heart rates. Some of the most deleterious effects are produced by simultaneous atrial and ventricular contraction, which results in continued suppression of cardiac output, both during tachycardias and at normal heart rates. Such situations are often highly symptomatic. Few measurements are available during external chest compression, and these suggest only marginal improvement in hemodynamics, with low pressures and output.
心律失常时的血流动力学效应可能由潜在病变（如梗死）以及心率或传导模式紊乱引起。在所有心律失常中，代偿机制倾向于恢复正常血流动力学，并且在左心室功能良好的情况下，尽管节律紊乱广泛，仍可实现这一点。异位搏动的血流动力学效应可导致每搏输出量急剧下降和心输出量减少，室性异位搏动比房性异位搏动的这种情况更严重。如果起源于房性而非室性，长时间的心动过速甚至在更高的心率（180次/分钟）时也能耐受。即使收缩压和心输出量降低，平均血压通常仍能维持。即使在健康的年轻受试者中，过快的心率也可能诱发心肌缺血。一些最有害的效应是由心房和心室同时收缩产生的，这会导致在心动过速期间和正常心率时心输出量持续受到抑制。这种情况通常症状很明显。在胸外按压期间可获得的测量数据很少，这些数据仅表明血流动力学有轻微改善，压力和输出量都很低。
