Collapsibility of caval vessels and right ventricular afterload: decoupling of stroke volume variation from preload during mechanical ventilation

Author(s):  
Elisa Valenti ◽  
Per Werner Moller ◽  
Jukka Takala ◽  
David Christian Berger

Background: Collapsibility of caval vessels and stroke volume and pulse pressure variations (SVV, PPV) are used as indicators of volume responsiveness. Their behavior under increasing airway pressures and changing right ventricular afterload is incompletely understood. If the phenomena of SVV and PPV augmentation are manifestations of decreasing preload, they should be accompanied by decreasing transmural right atrial pressures. Methods: Eight healthy pigs equipped with ultrasonic flow probes on the pulmonary artery were exposed to positive end-expiratory pressure of 5 and 10 cmH2O and three volume states (Euvolemia, defined as SVV < 10%, Bleeding and Retransfusion). SVV and PPV were calculated for the right and PPV for the left side of the circulation at increasing inspiratory airway pressures (15, 20, 25 cmH2O). Right ventricular afterload was assessed by surrogate flow profile parameters. Transmural pressures in the right atrium and the inferior and superior caval vessels (IVC and SVC) were determined. Results: Increasing airway pressure led to increases in ultrasonic surrogate parameters of right ventricular afterload, increasing transmural pressures in the right atrium and SVC, and a drop in transmural IVC pressure. SVV and PPV increased with increasing airway pressure, despite the increase in right atrial transmural pressure. Right ventricular stroke volume variation correlated with indicators of right ventricular afterload. This behavior was observed in both PEEP levels and all volume states. Conclusions: Stroke volume variation may reflect changes in right ventricle afterload, rather than changes in preload.

2007 ◽  
Vol 17 (5) ◽  
pp. 545-547 ◽  
Author(s):  
Frederik A. du Plessis ◽  
Willem A. Helbing ◽  
Ad J.J.C. Bogers

AbstractWe report on the management of Candida endocarditis in a 5-month old infant. The orifice of the tricuspid valve was totally obstructed, and the tension apparatus of the valve destroyed. Excision of the valve led to severe failure of the right heart. The combined use of anti-failure treatment, and reduction of right ventricular afterload with oxygen, nitric oxide and sildenafil, proved successful.


Circulation ◽  
2005 ◽  
Vol 112 (9_supplement) ◽  
Author(s):  
Sydney L. Gaynor ◽  
Hersh S. Maniar ◽  
Jeffrey B. Bloch ◽  
Paul Steendijk ◽  
Marc R. Moon

Background— Increased mortality in patients with chronic pulmonary hypertension has been associated with elevated right atrial (RA) pressure. However, little is known about the effects of chronic right ventricular (RV) pressure overload on RA and RV dynamics or the adaptive response of the right atrium to maintain RV filling. Methods and Results— In 7 dogs, RA and RV pressure and volume (conductance catheter) were recorded at baseline and after 3 months of progressive pulmonary artery banding. RA and RV elastance (contractility) and diastolic stiffness were calculated, and RA reservoir and conduit function were quantified as RA inflow with the tricuspid valve closed versus open, respectively. With chronic pulmonary artery banding, systolic RV pressure increased from 34±7 to 70±17 mm Hg ( P <0.001), but cardiac output did not change ( P >0.78). RV elastance and stiffness both increased ( P <0.05), suggesting preserved systolic function but impaired diastolic function. In response, RA contractility improved (elastance increased from 0.28±0.12 to 0.44±0.13 mm Hg/mL; P <0.04), and the atrium became more distensible, as evidenced by increased reservoir function (49±14% versus 72±8%) and decreased conduit function (51±14% versus 28±8%; P <0.002). Conclusions— With chronic RV pressure overload, RV systolic function was preserved, but diastolic function was impaired. To compensate, RA contractility increased, and the atrium became more distensible to maintain filling of the stiffened ventricle. This compensatory response of the right atrium likely plays an important role in preventing clinical failure in chronic pulmonary hypertension.


2003 ◽  
Vol 284 (1) ◽  
pp. H350-H357 ◽  
Author(s):  
Hersh S. Maniar ◽  
Sunil M. Prasad ◽  
Sydney L. Gaynor ◽  
Celeste M. Chu ◽  
Paul Steendijk ◽  
...  

Optimization of right atrial (RA) mechanics is important for maintaining right ventricular (RV) filling and global cardiac output. However, the impact of pericardial restraint on RA function and the compensatory role of the right atrium to changes in RV afterload remain poorly characterized. In eight open-chest sheep, RA elastance (contractility) and chamber stiffness were measured (RA pressure-volume relations) at baseline and during partial pulmonary artery (PA) occlusion. Data were collected before and after pericardiotomy. With the pericardium intact and partial PA occlusion, RA elastance increased by 28% ( P < 0.04), whereas RA stiffness tended to rise ( P = 0.08). However, after pericardiotomy, there was a significant fall in both RA elastance (54%, P < 0.04) and stiffness (39%, P < 0.04), and subsequent PA occlusion failed to induce a change in elastance ( P > 0.19) or stiffness ( P > 0.84). After pericardiotomy, RA elastance and stiffness fell dramatically, and the compensatory response of the right atrium to elevated RV afterload was lost. The ability of the right atrium to respond to changes in RV hemodynamics is highly dependent on pericardial integrity.


2005 ◽  
Vol 288 (5) ◽  
pp. H2140-H2145 ◽  
Author(s):  
Sydney L. Gaynor ◽  
Hersh S. Maniar ◽  
Sunil M. Prasad ◽  
Paul Steendijk ◽  
Marc R. Moon

The purpose of this study was to investigate the relationship between right atrial (RA) reservoir and conduit function and to determine how hemodynamic changes influence this relationship and its impact on cardiac output. In 11 open-chest sheep, RA reservoir and conduit function were quantified as RA inflow with the tricuspid valve closed versus open, respectively. Conduit function was separated into early (before A wave) and late (after A wave) components. The effects of inotropic stimulation, partial pulmonary artery occlusion, and pericardiotomy were tested. At baseline with the pericardium intact, reservoir function accounted for 0.56 (SD 0.13) of RA inflow, early conduit for 0.29 (SD 0.07), and late conduit (during RA contraction) for 0.16 (SD 0.11). Inotropic stimulation decreased conduit function and increased reservoir function, but these effects did not reach statistical significance. With partial pulmonary artery occlusion, early conduit function fell to 0.20 (SD 0.11) ( P < 0.04), and the conduit-to-reservoir ratio decreased by 41% ( P < 0.03). Similarly, after pericardiotomy, early conduit function fell to 0.14 (SD 0.09) ( P < 0.004), reservoir function increased to 0.72 (SD 0.08) ( P < 0.04), and, consequently, the early conduit-to-reservoir ratio decreased by 63% ( P < 0.006). Cardiac output was inversely related to the conduit-to-reservoir ratio ( r = 0.39, P < 0.001). This study demonstrated that the right atrium adjusts its ability to act more as a reservoir than a conduit in a dynamic manner. The RA conduit-to-reservoir ratio was directly related to the right ventricular pressure-RA pressure gradient at the time of maximum RA volume, with increased ventricular pressures favoring conduit function, but it was inversely related to cardiac output, with an increase in the reservoir contribution favoring improved cardiac output.


1999 ◽  
Vol 87 (5) ◽  
pp. 1644-1650 ◽  
Author(s):  
Antoine Vieillard-Baron ◽  
Yann Loubieres ◽  
Jean-Marie Schmitt ◽  
Bernard Page ◽  
Olivier Dubourg ◽  
...  

In a context such as acute respiratory distress syndrome, where optimum tidal volume and airway pressure levels are debated, the present study was designed to differentiate the right ventricular (RV) consequences of increasing lung volume from those secondary to increasing airway pressure during tidal ventilation. The study was conducted by combined two-dimensional echocardiographic and Doppler studies in 10 patients requiring mechanical ventilation in the controlled mode because of acute respiratory failure. Continuous monitoring of airway pressure on echocardiographic and Doppler recordings provided accurate timing of each cardiac event during the respiratory cycle, with particular attention being paid to end-expiratory and end-inspiratory atrial diameters, RV dimensions, and pulmonary artery and tricuspid flow estimated by the velocity-time integral (PAVTIand TVTI, respectively). At baseline, lung inflation during the inspiratory phase of mechanical ventilation produced a drop in PAVTIfrom 14.3 ± 2.6 cm at end expiration to 11.3 ± 2.1 cm at end inspiration. This drop occurred without reduction in right atrial diameter or in RV diastolic dimensions. It was not preceded but was followed by a decrease in TVTI, thus confirming an increase in RV outflow impedance. Manipulation of tidal volume without changing airway pressure and manipulation of airway pressure without changing tidal volume demonstrated that tidal volume, but not airway pressure, was the main determinant factor of RV afterloading during mechanical ventilation.


Critical Care ◽  
2010 ◽  
Vol 14 (6) ◽  
pp. 451 ◽  
Author(s):  
Frederic Michard ◽  
Guy Richards ◽  
Matthieu Biais ◽  
Marcel Lopes ◽  
Jose Auler

2005 ◽  
Vol 8 (2) ◽  
pp. 96 ◽  
Author(s):  
Osman Tansel Dar�in ◽  
Alper Sami Kunt ◽  
Mehmet Halit Andac

Background: Although various synthetic materials and pericardium have been used for atrial septal defect (ASD) closure, investigators are continuing to search for an ideal material for this procedure. We report and evaluate a case in which autologous right atrial wall tissue was used for ASD closure. Case: In this case, we closed a secundum ASD of a 22-year-old woman who also had right atrial enlargement due to the defect. After establishing standard bicaval cannulation and total cardiopulmonary bypass, we opened the right atrium with an oblique incision in a superior position to a standard incision. After examining the secundum ASD, we created a flap on the inferior rim of the atrial wall. A stay suture was stitched between the tip of the flap and the superior rim of the defect, and suturing was continued in a clockwise direction thereafter. Considering the size and shape of the defect, we incised the inferior attachment of the flap, and suturing was completed. Remnants of the flap on the inferior rim were resected, and the right atrium was closed in a similar fashion. Results: During an echocardiographic examination, neither a residual shunt nor perigraft thrombosis was seen on the interatrial septum. The patient was discharged with complete recovery. Conclusion: Autologous right atrial patch is an ideal material for ASD closure, especially in patients having a large right atrium. A complete coaptation was achieved because of the muscular nature of the right atrial tissue and its thickness, which is a closer match to the atrial septum than other materials.


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