Modified Glenn connection for acutely ischemic right ventricular failure reverses secondary left ventricular dysfunction

Danton, Mark; Byrne, John G.; Flores, Kathryn Q.; Hsin, Michael; Martin, Jeffrey S.; Laurence, Rita G.; Cohn, Lawrence H.; Aklog, Lishan

doi:10.1067/mtc.2001.114632

Cited by 27 publications

(25 citation statements)

References 33 publications

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“…66 These effects may be clinically relevant when the RV is volume unloaded by placement of a caval pulmonary shunt. Danton et al 67 showed experimentally that acute RV ischemia induced by coronary artery ligation induced LV dysfunction as measured by end-systolic elastance, a load-independent measure of LV contractility. LV dysfunction secondary to RV ischemia was reversed by the addition of a caval pulmonary shunt with restoration of LV end-systolic elastance.…”

Section: March 4 2014mentioning

confidence: 99%

Right Versus Left Ventricular Failure

2014

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1033V entricular failure manifests in many forms, its underlying physiology ranging from overt left ventricular (LV) systolic dysfunction to isolated right ventricular (RV) diastolic dysfunction, and the wide portfolio of resulting symptoms vary from chronic fluid retention to acute multiorgan dysfunction and death. In this review, we discuss the morphological, functional, and molecular similarities and differences in RV and LV responses to adverse loading and failure. We further discuss whether LV and RV function and failure can truly be discussed as separate entities and thereby examine interactions between the ventricles that on one hand contribute to ventricular dysfunction but on the other may be harnessed for therapeutic benefit. Embryological and Physiological Differences Between the RV and LVThe RV and LV have different embryological origins.1 The LV originates from the primary heart field; the RV, from the secondary heart field. Consequently, several genes specifically control RV formation, including, among others, Hand2 and Tbx20.2 During gestation, the RV functions as the systemic ventricle ( Figure 1A). During fetal life, in addition to supplying the modest amount of pulmonary blood flow, the RV pumps blood to the lower body and placenta and contributes more than half of the combined cardiac output.3 With the transition from fetal to postnatal physiology and with the reduction in pulmonary vascular resistance, the subpulmonary RV transforms its morphology and geometry, becoming a thin-walled chamber to adopt its postnatal physiological characteristics. 4 Because it faces a low impedance pulmonary circulation, the normal postnatal RV maintains a cardiac output equal to that of the LV at approximately a fifth of the energy cost. The trapezoidal RV pressure-volume loop reflects this difference, with few if any isovolumic periods. Consequently, RV output starts early during pressure generation and is later maintained by a "hangout period" when antegrade flow continues into the pulmonary artery despite the onset of RV relaxation.5 In contrast, the rectangular LV pressure-volume loops reflect the LV square-wave pump function with distinct and well-developed isovolumic contraction and relaxation periods.6 Likewise, RV myocytes display faster twitch velocities than LV myocytes. 7The physiological differences are reflected in morphological differences between the ventricles (Table 1). The low-pressure RV is triangular in the sagittal plane and crescent-shaped in cross section as a result of the concave RV free wall and convex interventricular septum wrapping around the high-pressured, thick-walled, bullet-shaped LV. Consequently, although the normal RV has a lower ratio of volume to surface area and a thinner wall than the LV, 8 the low cavity pressure determines a lower wall stress and lower oxygen demands.Anatomic differences are also apparent in myocardial architecture. LV subepicardial and subendocardial fibers are oblique and helical with fiber angles ranging from 30° to 80° with a mean of ≈60°, whereas ...

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Section: March 4 2014mentioning

confidence: 99%

Right Versus Left Ventricular Failure

2014

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“…8 Right ventricular preload reduction using a Glenn Shunt reduced RV volume and pressure, normalized the IVS position during diastole, and increased LV filling and ejection and systemic blood pressure. 8 In another RV infarct model using different loading conditions, the IVS was noted to paradoxically 'bulge' toward the RV free wall at the onset of ventricular systole (PVSM) causing an increase in RV dP/dt, a reduction in RV volume, and forward ejection of blood from the RV. 10,11,30 These authors speculated that the systolic pressure increase in the normally functioning LV was unopposed by the reduced pressure generation in the depressed RV, thereby increasing the left-to-right pressure gradient across the IVS.…”

Section: Lv-rv Interaction and The Ivsmentioning

confidence: 97%

“…[3][4][5][6] This left to right ''ventricular assistance'' is influenced by RV volume and pressure and the transseptal pressure gradient. 7,8 The clinical impact of this interaction increases with increasing RV dysfunction. [4][5][6][8][9][10][11] A number of investigations describe this interventricular interaction in terms of the IVS position, highlighting its impact on both LV and RV functions.…”

Section: Résumémentioning

confidence: 99%

“…[4][5][6][8][9][10][11] A number of investigations describe this interventricular interaction in terms of the IVS position, highlighting its impact on both LV and RV functions. [4][5][6][8][9][10][11] With the patient's informed consent, we present a case of severe primary RV failure that was successfully resuscitated with no significant improvement in the systolic function of the primary RV myocardial tissues. Of note, was the occurrence of paradoxical ventricular systolic septal motion (PVSM), during which the IVS moved toward the RV free wall during systole and appeared to contribute substantially to RV ejection.…”

Section: Résumémentioning

confidence: 99%

“…4,6,[8][9][10][11] In an acute RV free wall infarct model, elevated RV pressure and volume throughout the cardiac cycle caused a leftward shift of the IVS, resulting in both LV diastolic and systolic dysfunction. 8 Right ventricular preload reduction using a Glenn Shunt reduced RV volume and pressure, normalized the IVS position during diastole, and increased LV filling and ejection and systemic blood pressure. 8 In another RV infarct model using different loading conditions, the IVS was noted to paradoxically 'bulge' toward the RV free wall at the onset of ventricular systole (PVSM) causing an increase in RV dP/dt, a reduction in RV volume, and forward ejection of blood from the RV.…”

Section: Lv-rv Interaction and The Ivsmentioning

confidence: 99%

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Case report: paradoxical ventricular septal motion in the setting of primary right ventricular myocardial failure

Maslow

Schwartz

Mahmood

et al. 2009

Can J Anesth/J Can Anesth

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Purpose In this report, a case of right ventricular (RV) failure, hemodynamic instability, and systemic organ failure is described to highlight how paradoxical ventricular systolic septal motion (PVSM), or a rightward systolic displacement of the interventricular septum, may contribute to RV ejection. Clinical features Multiple inotropic medications and vasopressors were administered to treat right heart failure and systemic hypotension in a patient following combined aortic and mitral valve replacement. In the early postoperative period, echocardiographic evaluation revealed adequate left ventricular systolic function, akinesis of the RV myocardial tissues, and PVSM. In the presence of PVSM, RV fractional area of contraction was C35% despite akinesis of the primary RV myocardial walls. The PVSM appeared to contribute toward RV ejection. As a result, the need for multiple inotropes was re-evaluated, in considering that end-organ dysfunction was the result of systemic hypotension and prolonged vasopressor administration. After discontinuation of phosphodiesterase inhibitors, native vascular tone returned and the need for vasopressors declined. This was followed by recovery of systemic organ function. Echocardiographic re-evaluation two years later, revealed persistent akinesis of the RV myocardial tissues and PVSM, the latter appearing to contribute toward RV ejection. Conclusions This case highlights the importance of left to RV interactions, and how PVSM may mediate these hemodynamic interactions. RésuméObjectif Dans ce compte-rendu, un cas de de´faillance ventriculaire droite (VD), d'instabilite´he´modynamique et de de´faillance organique syste´mique est de´crit afin de souligner la manie`re dont le mouvement systolique paradoxal du septum interventriculaire (PVSM), ou un de´placement systolique de la cloison interventriculaire vers la droite, peut jouer un rôle dans l'e´jection du VD. É léments cliniques De nombreux me´dicaments inotropes et vasopresseurs ont e´te´administre´s pour traiter une de´faillance cardiaque droite ainsi qu'une hypotension syste´mique chez un patient a`la suite d'une chirurgie valvulaire aortique et mitrale combine´e. Au de´but de la pe´riode postope´ratoire, l'e´valuation e´chocardiographique a re´ve´le´une fonction systolique ade´quate du ventricule Electronic supplementary material The online version of this article

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Physiology

Shabetai

2003

The Pericardium

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Modified Glenn connection for acutely ischemic right ventricular failure reverses secondary left ventricular dysfunction

Abstract: Right ventricular ischemia-induced dilation resulted in acute impairment of left ventricular contractility and relaxation. A modified Glenn shunt attenuated the left ventricular dysfunction by limiting right ventricular dilation and restoring left ventricular cavity geometry.

Cited by 27 publications

References 33 publications

Right Versus Left Ventricular Failure

Right Versus Left Ventricular Failure

Case report: paradoxical ventricular septal motion in the setting of primary right ventricular myocardial failure

Physiology

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