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严重高血压和心动过缓的一个意外原因:超声心动图血流动力学评估的作用。

An Unexpected Cause of Severe Hypertension and Bradycardia: The Role of Hemodynamic Assessment by Echocardiography.

作者信息

Myrmel Gard M S, Ali Abukar, Lunde Torbjørn, Mancia Giuseppe, Saeed Sahrai

机构信息

Department of Heart Disease, Haukeland University Hospital, Bergen, Norway.

Milano and Policlinico di Monza, University of Milano-Bicocca, Monza, Italy.

出版信息

Pulse (Basel). 2022 Jun 14;10(1-4):46-51. doi: 10.1159/000525078. eCollection 2022 Dec.

Abstract

Severe hypertension has numerous etiologies. When accompanied by bradycardia, the spectrum of differential diagnoses is greatly narrowed and is commonly seen in patients with increased intracranial pressure. However, other etiologies such as bradycardia-induced hypertension are rarely mentioned. Here we report the case of a 73-year-old woman presenting with symptoms of heart failure, severe hypertension, and bradycardia with a 2:1 atrioventricular block. Echocardiography demonstrated increased left ventricular filling secondary to bradycardia and prolonged diastole, leading to greater ventricular stretch, increased contractile force and greater stroke volume (Frank-Starling mechanism), which subsequently caused elevated systolic blood pressure (BP), low diastolic BP and a wide pulse pressure. Treating the bradycardia by pacing led to an immediate and substantial BP reduction, although complete BP normalization had a slower time course and was probably due to the concomitant effect of the antihypertensive treatment initiation. This pathophysiological mechanism has received little attention in the literature. Further, stimulation of sympathetic afferents located in the heart by distension of the cardiac walls as well as the role of vagally innervated cardiopulmonary receptors due to the increased pressure in the heart and the pulmonary artery should also be kept in mind as alternative hypotheses.

摘要

重度高血压有多种病因。当伴有心动过缓时,鉴别诊断范围会大大缩小,常见于颅内压升高的患者。然而,其他病因如心动过缓诱发的高血压很少被提及。在此,我们报告一例73岁女性患者,其表现为心力衰竭、重度高血压以及伴有2:1房室传导阻滞的心动过缓。超声心动图显示,由于心动过缓和舒张期延长,左心室充盈增加,导致心室更大程度的拉伸、收缩力增加和更大的每搏输出量(Frank-Starling机制),进而引起收缩压升高、舒张压降低和脉压增宽。通过起搏治疗心动过缓导致血压立即大幅下降,尽管血压完全恢复正常的过程较为缓慢,这可能是由于开始使用抗高血压治疗的协同作用。这种病理生理机制在文献中很少受到关注。此外,心脏壁扩张对位于心脏的交感传入神经的刺激以及由于心脏和肺动脉压力升高导致的迷走神经支配的心肺感受器的作用,也应作为替代假说来考虑。

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