Zoccali C, Tripepi G, Mallamaci F, Panuccio V
CNR Centro di Fisiologia Clinica, Bianchi e Morelli, Reggio Cal, Italy.
Nephrol Dial Transplant. 1997 Mar;12(3):519-23. doi: 10.1093/ndt/12.3.519.
Hypotension during haemodialysis may be caused by the activation of a cardiovascular reflex causing abrupt sympathetic withdrawal, vasodilatation and bradycardia (bradycardic hypotension). However, the frequency of this type of hypotension is undefined and it is unclear whether or not it underlies a peculiar predisposition to vasodepressor syncope.
To assess the prevalence of bradycardic hypotension and to test the hypothesis that dialysis patients are predisposed to vasodepressor syncope.
Sixty hypotensive episodes were recorded in 20 patients (> or = 2 episodes in 15 patients). Heart rate increased in 35 episodes, did not change in 19 episodes and decreased in six episodes. The HR response pattern to hypotension was reproducible in 10 patients (always tachycardia, 6; always unchanged heart rate 4). Patients developing bradycardic hypotension (n = 5) all had an erratic HR response to hypotension (i.e. bradycardia preceded or followed by tachycardia or by no HR change) and were characterized either by the typical haemodynamic pattern of hypovolaemia (predialysis hypotension, tachycardia and low TBW) or by being treated with a very high UF rate (> 0.3 ml/kg/min). Post-dialysis echocardiography showed that the LVEDD was less (one-tailed P = 0.055) in patients with bradycardic hypotension than in those with tachycardic responses or with unchanged HR. On tilt testing (after dialysis) three of 11 (27%) dialysis hypotensive patients developed bradycardic hypotension. This proportion was identical to that expected in healthy subjects and in control patients without syncope.
Tachycardia is the more frequent heart rate response to dialysis hypotension in uraemic patients. Bradycardic hypotension in dialysis patients is associated with a haemodynamic profile indicating a more severe degree of cardiovascular underfilling. Bradycardic hypotension probably represents a physiological response to hypovolaemia rather than the expression of a peculiar predisposition to vasodepressor syncope.
血液透析期间的低血压可能由心血管反射激活引起,导致突然的交感神经撤离、血管舒张和心动过缓(心动过缓性低血压)。然而,这种类型低血压的发生率尚不明确,且不清楚它是否是血管减压性晕厥特殊易感性的基础。
评估心动过缓性低血压的患病率,并检验透析患者易患血管减压性晕厥这一假设。
20例患者记录到60次低血压发作(15例患者发作≥2次)。35次发作时心率增加,19次发作时心率不变,6次发作时心率降低。10例患者对低血压的心率反应模式可重复(6例总是心动过速,4例心率始终不变)。发生心动过缓性低血压的患者(n = 5)对低血压的心率反应均不稳定(即心动过缓之前或之后伴有心动过速或心率无变化),其特征要么是典型的血容量不足血流动力学模式(透析前低血压、心动过速和低总体水量),要么是超滤率非常高(> 0.3 ml/kg/min)。透析后超声心动图显示,心动过缓性低血压患者的左心室舒张末期内径小于心动过速反应或心率不变患者(单尾P = 0.055)。在倾斜试验(透析后)中,11例透析低血压患者中有3例(27%)发生心动过缓性低血压。该比例与健康受试者和无晕厥的对照患者预期比例相同。
心动过速是尿毒症患者对透析低血压更常见的心率反应。透析患者的心动过缓性低血压与血流动力学特征相关,提示心血管充盈不足程度更严重。心动过缓性低血压可能代表对血容量不足的生理反应,而非血管减压性晕厥特殊易感性的表现。