Transseptal pressure gradient with leftward septal displacement during the Mueller manoeuvre in man.

Guzman, Pablo A.; Maughan, W L; Yin, F. C. P.; Eaton, Leland W.; Brinker, Jeffrey A.; Weisfeldt, Myron L.; Weiss, J. L.

doi:10.1136/hrt.46.6.657

Cited by 79 publications

(27 citation statements)

References 19 publications

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“…These changes were far less striking than the end-diastolic flattening seen during bypass or cardiac arrest, but are consistent with findings of previous studies that indicated persistent septal flattening throughout several cardiac cycles.1 2 Why the septum maintains its flat configuration during systole when the left ventricular cavity pressure greatly exceeds right ventricular pressure is not known. As ventricular contraction proceeds, the stiffness of the muscle increases above the level present during diastole, when it is more flaccid.9' 10 Thus, one possible explanation for the persistent systolic flattening is that the increase in stiffness in the initially flattened septum is enough to counterbalance the increase in left-to-right forces tending to push the septum toward the right ventricle.…”

Section: Resultssupporting

confidence: 89%

Septal geometry in the unloaded living human heart.

et al. 1986

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Right ventricular loading leads to diastolic septal flattening in man without necessarily requiring right ventricular pressure to exceed left ventricular pressure. This observation suggested that the unstressed septal configuration is flat and that its normal concave shape is due to the left-to-right transseptal pressure gradient. To examine this hypothesis, we studied septal configuration by twodimensional echocardiography in nine patients with normal global and regional left ventricular function during surgery for coronary artery disease. (CA). There were no changes in any measurements between C and OP or between CPB and CA. Left ventricular end-diastolic cavity area decreased from 16.5 + 2.1 cm2 at C to 11.1 + 4.5 cm2 after CPB, and further decreased to 8.9 + 3.5 cm2 after CA (p < .001), yet the septum flattened, as shown by an increase in its radius of curvature from 1.7 0.5 cm during C to 2.5 0.7 cm after CPB, and to 2.9 + 1.0 cm after CA (p < .001), or from 0.4 0.1 to 0.8 0.4 to 1.1 0.5 U (p < .001) when normalized for cavity area. Diastolic transseptal pressure gradient was reduced from 4.1 ± 2.3 mm Hg during C to 1. 1 ± 1.8 mm Hg after CPB, and to 0.5 ± 1.4 mm Hg after CA (p < .01). Thus, in the unloaded human heart, the interventricular septum is more flat and occupies a neutral position between the left and right ventricle. Septal flattening due to a reduced but not reversed transseptal left-to-right gradient results from assumption of this unstressed shape as the right ventricular end-diastolic pressure approaches the left ventricular end-diastolic pressure. Circulation 74, No. 3, 463-468, 1986. OWING TO its anatomic position, the interventricular septum is postulated to be a mediator of ventricular interaction. 1-5 However, the mechanisms underlying the changes in septal position are still unclear. Previous work from our laboratory demonstrated leftward displacement of the interventricular septum with acute right ventricular loading during a Mueller maneuver in humans (a forced inspiration against a closed airway). 1 In an effort to determine whether these shifts occurred as a result of right ventricular diastolic pressure exceeding left ventricular diastolic pressures, we then measured the diastolic transseptal pressure gradient during the Mueller maneuver, and correlated these changes with alterations in septal geometry. This study (again in humans) showed that the septal flattening that occurs with acute right ventricular loading is accompanied by a decrease in the diastolic left-to-right transseptal pressure gradient, without requiring a reversal of this gradient.2 This raised the possibility that the reason why the interventricular septum shifts leftward during acute right ventricular loading is that the normal septal configuration in the unloaded heart is flat, and that in the working heart it is held in its usual position concave to the left ventricular cavity by the normal and persistent left-to-right positive transseptal pressure gradient. The goal of the current study was to de...

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Section: Resultssupporting

confidence: 89%

Septal geometry in the unloaded living human heart.

et al. 1986

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“…These results are similar to those we previously reported1' in experiments during pulmonary artery constriction, are similar to the studies of others, 3,20,2' and are in general agreement with our current understanding of diastolic septal mechanics. [25][26][27] The importance of the contribution of pericardial constraint to the mechanism of the shift has been emphasized previously; opening the pericardium results in less septal shift than occurs while the pericardium is intact.1 7} 28 Our data differ from those in a recent report that concluded that septal shift was not an important factor in the reduction of LV volume in dogs with pulmonary vascular injury induced by glass beads." The degree of elevation of RV diastolic pressure in that study suggests that a septal shift was not observed because the increase in RV afterload was not as great as that produced by the repeated embolization in our study.…”

Section: Transseptal Pressure Gradientcontrasting

confidence: 57%

Ventricular interaction during experimental acute pulmonary embolism.

et al. 1988

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Although stroke volume may decrease markedly after acute pulmonary embolism, left ventricular end-diastolic pressure (LVEDP) usually changes very little, which suggests that compliance or contractility or both are reduced. To test the hypothesis that the altered LV function during pulmonary embolism is primarily due to reduced preload mediated by increased pericardial constraint, hemodynamics and chamber dimensions (measured by sonomicrometry) were assessed in seven anesthetized dogs during control volume loading, after pulmonary embolism (with autologous blood clot), and after repeated pulmonary embolism in the volume-loaded state. The correlation between LVEDP and an index of LVED volume (LVED area index) throughout a wide range of LVEDP before and after embolism was poor (mean r= 0.42; range, 0-0.82). However, the correlation between transmural LVEDP (LVEDP -directly measured pericardial pressure) and LVED area index (mean r = 0.78; range, 0.61-0.94) was significantly higher (p=0.03). Similarly, an index of stroke work (LV area stroke work) correlated less well (p<0.01) with LVEDP (mean r=0.43; range, 0.07-0.77) than with transmural LVEDP (mean r=0.82; range, 0.68-0.92). LV area stroke work also correlated well with the LV area index (mean r = 0.84; range, 0.70-0.95). These data indicate that neither compliance nor contractility is substantially altered during acute pulmonary embolism. The altered LV performance is due to reduced LV preload as reflected by a decrease in transmural LVEDP. This study also demonstrates that LVEDP is a poor index of LV preload during pulmonary embolism, whereas transmural LVEDP accurately reflects LVED dimensions. (Circulation 1988;78:761-768) H emodynamic effects of acute pulmonary embolism include increased pulmonary artery and right ventricular (RV) pressures, and when embolism is severe, the effects include decreased cardiac output, systemic hypotension, and death.1-9 The reduction in stroke volume has been attributed to reduced left ventricular end-diastolic (LVED) volume.910 However, LV filling pressure is usually altered only slightly and may even increase,34,7 which suggests that pulmonary embolism may result in decreased LV compliance or contractility or both.Based on earlier studies from our laboratory1ll12and from other laboratories,10,13-2' we hypothesized

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“…12 13 The increase in the right atrial "x" descent reflects a "suction" effect transmitted to the slack atrium after atrial systole by the strongly negative intrathoracic pressure. The right ventricular to right atrial pressure difference was therefore greater during the Mueller maneuver and this, along with the altered right Vol.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamics of the Mueller maneuver in man: right and left heart micromanometry and Doppler echocardiography.

et al. 1987

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Ten subjects with normal hemodynamics were studied during elective cardiac catheterization with right and left heart multisensor micromanometry to assess hemodynamic responses to the Mueller maneuver. Simultaneous right and left circulatory hemodynamics and left ventricular, pulmonary arterial, and aortic pressures were recorded, in addition to pulmonary arterial and aortic flow velocities. Steady-state cardiac outputs were determined by thermal dilution. Aortic systolic and mean pressures were not significantly changed during the Mueller maneuver, in contrast to a lower diastolic (p = .019) and higher pulse pressure (p = .016). Mean right atrial pressure (± SE) decreased from 7 1 to -17 + 4 mm Hg (p = .0002) and the right atrial "x" descent was markedly accentuated. Left ventricular end-diastolic pressure decreased from 12 + 4 to -3 ± 13 mm Hg (p = .0025). Systemic vascular resistance and left ventricular peak positive dP/dt were increased during the Mueller maneuver (p < .02), cardiac output and stroke volume were reduced (p < .05), and there was no significant change in heart rate. Right and left peak flow velocities showed a trend toward a bilateral decrease (right, p = .054; left, p > .1), and times to peak flow velocity were increased in the pulmonary artery (p = .007) and reduced in the aortic root (p = .03). Normal subjects were studied separately by pulsed Doppler echocardiography. During the sustained Mueller maneuver, the internal jugular and right ventricular dimensions decreased, and superior vena cava Doppler flow was reduced. These data demonstrate reduced flow through the right and left heart chambers during a sustained Mueller maneuver in humans, in contrast to prior theory and animal data suggesting that right heart flow is increased during sustained forced inspiratory effort.

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Transseptal pressure gradient with leftward septal displacement during the Mueller manoeuvre in man.

Cited by 79 publications

References 19 publications

Septal geometry in the unloaded living human heart.

Septal geometry in the unloaded living human heart.

Ventricular interaction during experimental acute pulmonary embolism.

Hemodynamics of the Mueller maneuver in man: right and left heart micromanometry and Doppler echocardiography.

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