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Right over left ventricular end-diastolic area relevance to predict hemodynamic intolerance of high-frequency oscillatory ventilation in patients with severe ARDS.

ABSTRACT: BACKGROUND:High-frequency oscillatory ventilation (HFOV) does not improve the prognosis of ARDS patients despite an improvement in oxygenation. This paradox may partly be explained by HFOV hemodynamic side-effects on right ventricular function. Our goal was to study the link between HFOV and hemodynamic effects and to test if the pre-HFOV right over left ventricular end-diastolic area (RVEDA/LVEDA) ratio, as a simple parameter of afterload-related RV dysfunction, could be used to predict HFOV hemodynamic intolerance in patients with severe ARDS. METHODS:Twenty-four patients were studied just before and within 3 h of HFOV using transthoracic echocardiography and transpulmonary thermodilution. RESULTS:Before HFOV, the mean PaO2/FiO2 ratio was 89 ± 23. The number of patients with a RVEDA/LVEDA ratio >0.6 significantly increased after HFOV [11 (46 %) vs. 17 (71 %)]. Although HFOV did not significantly decrease the arterial pressure (systolic, diastolic, mean and pulse pressure), it significantly decreased the cardiac index (CI) by 13 ± 18 % and significantly increased the RVEDA/LVEDA ratio by 14 ± 11 %. A significant correlation was observed between pre-HFOV RVEDA/LVEDA ratio and CI diminution after HFOV (r = 0.78; p < 0.0001). A RVEDA/LVEDA ratio superior to 0.6 resulted in a CI decrease >15 % during HFOV with a sensitivity of 80 % (95 % confidence interval 44-98 %) and a specificity of 79 % (confidence interval 49-95 %). CONCLUSION:The RVEDA/LVEDA ratio measured just before HFOV predicts the hemodynamic intolerance of this technique in patients with severe ARDS. A high ratio under CMV raises questions about the use of HFOV in such patients. TRIAL REGISTRATION:ClinicalTrials.gov: NCT01167621.

SUBMITTER: Ursulet L

PROVIDER: S-EPMC4573736 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature

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Right over left ventricular end-diastolic area relevance to predict hemodynamic intolerance of high-frequency oscillatory ventilation in patients with severe ARDS.

Ursulet Lionel L Roussiaux Arnaud A Belcour Dominique D Ferdynus Cyril C Gauzere Bernard-Alex BA Vandroux David D Jabot Julien J

Annals of intensive care 20150917 1

<h4>Background</h4>High-frequency oscillatory ventilation (HFOV) does not improve the prognosis of ARDS patients despite an improvement in oxygenation. This paradox may partly be explained by HFOV hemodynamic side-effects on right ventricular function. Our goal was to study the link between HFOV and hemodynamic effects and to test if the pre-HFOV right over left ventricular end-diastolic area (RVEDA/LVEDA) ratio, as a simple parameter of afterload-related RV dysfunction, could be used to predict ...[more]

PMID: 26380993

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Project description:Background and objectiveThe effect of chronic pulmonary regurgitation (PR) on right ventricular (RV) dysfunction in repaired Tetralogy of Fallot (RTOF) patients is well recognized by cardiac magnetic resonance (CMR). However, the link between RV wall motion, intracardiac flow and PR has not been established. Hemodynamic force (HDF) represents the global force exchanged between intracardiac blood volume and endocardium, measurable by 4D flow or by a novel mathematical model of wall motion. In our study, we used this novel methodology to derive HDF in a cohort of RTOF patients, exclusively using routine CMR imaging.MethodsRTOF patients and controls with CMR imaging were retrospectively included. Three-dimensional (3D) models of RV were segmented, including RV outflow tract (RVOT). Feature-tracking software (QStrain 2.0, Medis Medical Imaging Systems, Leiden, Netherlands) captured endocardial contours from long/short-axis cine and used to reconstruct RV wall motion. A global HDF vector was computed from the moving surface, then decomposed into amplitude/impulse of three directional components based on reference (Apical-to-Basal, Septal-to-Free Wall and Diaphragm-to-RVOT direction). HDF were compared and correlated against CMR and exercise stress test parameters. A subset of RTOF patients had 4D flow that was used to derive vorticity (for correlation) and HDF (for comparison against cine method).Results68 RTOF patients and 20 controls were included. RTOF patients had increased diastolic HDF amplitude in all three directions (p<0.05). PR% correlated with Diaphragm-RVOT HDF amplitude/impulse (r = 0.578, p<0.0001, r = 0.508, p < 0.0001, respectively). RV ejection fraction modestly correlated with global HDF amplitude (r = 0.2916, p = 0.031). VO2-max correlated with Septal-to-Free Wall HDF impulse (r = 0.536, p = 0.007). Diaphragm-to-RVOT HDF correlated with RVOT vorticity (r = 0.4997, p = 0.001). There was no significant measurement bias between Cine-derived HDF and 4D flow-derived HDF by Bland-Altman analysis.ConclusionRTOF patients have abnormal diastolic HDF that is correlated to PR, RV function, exercise capacity and vorticity. HDF can be derived from conventional cine, and is a potential link between RV wall motion and intracardiac flow from PR in RTOF patients.

Project description:Right ventricular (RV) diastolic function is impaired in patients with pulmonary arterial hypertension (PAH). Our previous study showed that elevated cardiomyocyte stiffness and myofilament Ca(2+) sensitivity underlie diastolic dysfunction in PAH. This study investigates protein modifications contributing to cellular diastolic dysfunction in PAH.RV samples from PAH patients undergoing heart-lung transplantation were compared to non-failing donors (Don). Titin stiffness contribution to RV diastolic dysfunction was determined by Western-blot analyses using antibodies to protein-kinase-A (PKA), C? (PKC?) and Ca(2+)/calmoduling-dependent-kinase (CamKII?) titin and phospholamban (PLN) phosphorylation sites: N2B (Ser469), PEVK (Ser170 and Ser26), and PLN (Thr17), respectively. PKA and PKC? sites were significantly less phosphorylated in PAH compared with donors (P<0.0001). To test the functional relevance of PKA-, PKC?-, and CamKII?-mediated titin phosphorylation, we measured the stiffness of single RV cardiomyocytes before and after kinase incubation. PKA significantly decreased PAH RV cardiomyocyte diastolic stiffness, PKC? further increased stiffness while CamKII? had no major effect. CamKII? activation was determined indirectly by measuring PLN Thr17phosphorylation level. No significant changes were found between the groups. Myofilament Ca(2+) sensitivity is mediated by sarcomeric troponin I (cTnI) phosphorylation. We observed increased unphosphorylated cTnI in PAH compared with donors (P<0.05) and reduced PKA-mediated cTnI phosphorylation (Ser22/23) (P<0.001). Finally, alterations in Ca(2+)-handling proteins contribute to RV diastolic dysfunction due to insufficient diastolic Ca(2+) clearance. PAH SERCA2a levels and PLN phosphorylation were significantly reduced compared with donors (P<0.05).Increased titin stiffness, reduced cTnI phosphorylation, and altered levels of phosphorylation of Ca(2+) handling proteins contribute to RV diastolic dysfunction in PAH.

Project description:BackgroundSevere right ventricular failure (RVF) after left ventricular assist device (LVAD) implantation increases morbidity and mortality. We investigated the association between intraoperative right heart hemodynamic data, echocardiographic parameters, and severe versus nonsevere RVF.MethodsA review of LVAD patients between March 2013 and March 2016 was performed. Severe RVF was defined by the need for a right ventricular mechanical support device, inotropic, and/or inhaled pulmonary vasodilator requirements for >14 days. From a chart review, the right ventricular failure risk score was calculated and right heart hemodynamic data were collected. Pulmonary artery pulsatility index (PAPi) [(pulmonary artery systolic pressure - pulmonary artery diastolic pressure)/central venous pressure (CVP)] was calculated for 2 periods: (1) 30 minutes before cardiopulmonary bypass (CPB) and (2) after chest closure. Echocardiographic data were recorded pre-CPB and post-CPB by a blinded reviewer. Univariate logistic regression models were used to examine the performance of hemodynamic and echocardiographic metrics.ResultsA total of 110 LVAD patients were identified. Twenty-five did not meet criteria for RVF. Of the remaining 85 patients, 28 (33%) met criteria for severe RVF. Hemodynamic factors associated with severe RVF included: higher CVP values after chest closure (18 ± 9 vs 13 ± 5 mm Hg; P = .0008) in addition to lower PAPi pre-CPB (1.2 ± 0.6 vs 1.7 ± 1.0; P = .04) and after chest closure (0.9 ± 0.5 vs 1.5 ± 0.8; P = .0008). Post-CPB echocardiographic findings associated with severe RVF included: larger right atrial diameter major axis (5.4 ± 0.9 vs 4.9 ± 1.0 cm; P = .03), larger right ventricle end-systolic area (22.6 ± 8.4 vs 18.5 ± 7.9 cm; P = .03), lower fractional area of change (20.2 ± 10.8 vs 25.9 ± 12.6; P = .04), and lower tricuspid annular plane systolic excursion (0.9 ± 0.2 vs 1.1 ± 0.3 cm; P = .008). Right ventricular failure risk score was not a significant predictor of severe RVF. Post-chest closure CVP and post-chest closure PAPi discriminated severe from nonsevere RVF better than other variables measured, each with an area under the curve of 0.75 (95% CI, 0.64-0.86).ConclusionsPost-chest closure values of CVP and PAPi were significantly associated with severe RVF. Echocardiographic assessment of RV function post-CPB was weakly associated with severe RVF.

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Right over left ventricular end-diastolic area relevance to predict hemodynamic intolerance of high-frequency oscillatory ventilation in patients with severe ARDS.

Publications

Right over left ventricular end-diastolic area relevance to predict hemodynamic intolerance of high-frequency oscillatory ventilation in patients with severe ARDS.

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