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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intraoperative correction of preload in patients with acquired valvular disease (AVD) complicated by right-ventricular failure and severe pulmonary hypertension necessitates search for pathogenetically based algorithms of anesthesiological strategy. The objective of this study was to develop a strategy of assessing and treating the preload at the stage of induction anesthesia in patients with right-ventricular failure. During surgery central hemodynamic parameters and their response to a short head-down-tilt (15-20 degrees) were evaluated in patients (n = 42) with cardiac index (CI) less than 2 l/min/m2 after induction anesthesia. The patients were divided into 2 groups with different severity of preoperative status. Group 1 (main) included 24 patients with stages II-III cardiac failure (according to N. Strazhesko and B. Vasilenko) and group 2 (control) consisted of 18 patients with stage IIA cardiac failure. Progressing preoperative cardiac failure resulted in decrease of cardiac index and failure of compensatory hemodynamic mechanisms in AVD patients. The level of right-ventricular preload, pulmonary resistance, and stroke index were lower in group 1 than in the controls; however, 8% of group 1 patients responded positively to increased preload. In the control group 50% responded favorably to head-down-tilt. Hence, comprehensive assessment of cardiac index, central hemodynamic parameters and their response to head-down tilt help individually choose the anesthesiological strategy.
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PMID:[The anesthesiological procedure for correcting preloading in the surgery of acquired mitral valve defects]. 1090 Jul 13

Lumped parameter models have been employed for decades to simulate important hemodynamic couplings between a left ventricular assist device (LVAD) and the native circulation. However, these studies seldom consider the pathological descending limb of the Frank-Starling response of the overloaded ventricle. This study introduces a dilated heart failure model featuring a unimodal end systolic pressure-volume relationship (ESPVR) to address this critical shortcoming. The resulting hemodynamic response to mechanical circulatory support are illustrated through numerical simulations of a rotodynamic, continuous flow ventricular assist device (cfVAD) coupled to systemic and pulmonary circulations with baroreflex control. The model further incorporated septal interaction to capture the influence of left ventricular (LV) unloading on right ventricular function. Four heart failure conditions were simulated (LV and bi-ventricular failure with/without pulmonary hypertension) in addition to normal baseline. Several metrics of LV function, including cardiac output and stroke work, exhibited a unimodal response whereby initial unloading improved function, and further unloading depleted preload reserve thereby reducing ventricular output. The concept of extremal loading was introduced to reflect the loading condition in which the intrinsic LV stroke work is maximized. Simulation of bi-ventricular failure with pulmonary hypertension revealed inadequacy of LV support alone. These simulations motivate the implementation of an extremum tracking feedback controller to potentially optimize ventricular recovery.
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PMID:Simulation of dilated heart failure with continuous flow circulatory support. 2446 11

Aortic counterpulsation (IABP) consists in an ECG-controlled forced deflation and inflation of a balloon positioned in the aorta. The device is designed to decrease the ventricular afterload during systole and to increase the coronary driving pressure during diastole. In biomechanical terms, the IABP improves the mechanical matching between the pump and the load, facilitating the transfer of ventricular energy. This paper describes a completely passive aortic counterpulsation solution, with an intra-aortic balloon without a pumping system, designed to improve the mechanical matching between the ventricle and the artery at very low cost and complexity. The only requirement is an external reservoir to amplify the balloon pulsations due to physiologic arterial pressure pulse. Using a cardiovascular simulator and changing the reservoir pressure, a systolic not negligible (7.8ml) gas volume exchange between the intra-aortic balloon and the reservoir was measured. The same cardiovascular simulator was used to demonstrate an increase in stroke volume in three conditions of progressive ventricular failure, by detecting a change in systolic and diastolic arterial pressures and stroke volume (SV). The maximal arterial pressure always decreased and the diastolic pressure increased. The SV increased up to 7.8%, demonstrating an arterial elastance reduction and better ventricular-aortic mechanical matching and energy transfer.
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PMID:Passive aortic counterpulsation: biomechanical rationale and bench validation. 2467 11


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