Miller M J, McKay R G, Ferguson J J, Sahagian P, Nakao S, Come P C, Grossman W
Circulation. 1986 Apr;73(4):799-808. doi: 10.1161/01.cir.73.4.799.
Pressure-volume relationships in the right atrium were examined before and after the creation of acute experimental tricuspid regurgitation in pigs. A 1.3 kHz multielectrode impedance catheter with a measuring current of 4 mA was used to determine instantaneous right atrial pressure and relative blood volume; right atrial dimension was assessed simultaneously with ultrasonic crystals attached to the atrial walls. Impedance volume waveforms and ultrasonic crystal dimensions closely paralleled each other at baseline and after the induction of tricuspid regurgitation. The normal right atrial pressure-volume plot exhibited a figure-of-eight configuration, with an "a-loop" and a "v-loop" corresponding to the a-wave and v-wave of the right atrial pressure tracing. With severe tricuspid regurgitation, atrial pump function was abolished, and the pressure-volume plot exhibited a single clockwise loop, consistent with complete ventricularization of the right atrium. Intermediate degrees of tricuspid regurgitation preserved the figure-of-eight loop, but the size of both the a-loop and the v-loop were increased, consistent with a Starling-type load imposed on the atrium by the regurgitant blood volume. Increased right ventricular afterload mediated by constriction of the pulmonary artery and infusion of methoxamine reversibly converted the right atrial pressure-volume loop from that of mild to that of severe tricuspid regurgitation. Alternatively, constriction of the inferior vena cava and infusion of nitroprusside changed the right atrial pressure-volume loop from that of a severe pattern of tricuspid regurgitation to a less severe type of pattern. Infusion of dobutamine increased the size of the a-loop relative to the v-loop both at baseline and after induction of tricuspid regurgitation. We conclude that tricuspid regurgitation induces changes in right atrial mechanics that can be detected and quantified with an impedance catheter.
在猪身上制造急性实验性三尖瓣反流前后，对右心房的压力-容积关系进行了研究。使用一根测量电流为4 mA的1.3 kHz多电极阻抗导管来测定右心房瞬时压力和相对血容量；通过附着在心房壁上的超声晶体同时评估右心房尺寸。在基线状态以及诱导三尖瓣反流后，阻抗容积波形和超声晶体尺寸彼此密切平行。正常的右心房压力-容积图呈现出8字形结构，其中“a环”和“v环”分别对应于右心房压力描记图中的a波和v波。严重三尖瓣反流时，心房泵功能丧失，压力-容积图呈现出单个顺时针环，这与右心房完全心室化一致。中度三尖瓣反流保留了8字形环，但a环和v环的大小均增加，这与反流血量对心房施加的斯塔林型负荷一致。通过肺动脉收缩和甲氧明输注介导的右心室后负荷增加，可使右心房压力-容积环从轻度三尖瓣反流状态可逆地转变为重度三尖瓣反流状态。相反，下腔静脉收缩和硝普钠输注可使右心房压力-容积环从重度三尖瓣反流模式转变为较轻的模式。在基线状态以及诱导三尖瓣反流后，多巴酚丁胺输注均增加了a环相对于v环的大小。我们得出结论，三尖瓣反流会引起右心房力学变化，这些变化可用阻抗导管进行检测和量化。
