Aortic dP/dtmax accurately reflects left ventricular contractility when effective preload independence is achieved

peer reviewe

Runtime and aPTT predict venous thrombosis and thromboembolism in patients on extracorporeal membrane oxygenation: a retrospective analysis

BACKGROUND: Even though bleeding and thromboembolic events are major complications of extracorporeal membrane oxygenation (ECMO), data on the incidence of venous thrombosis (VT) and thromboembolism (VTE) under ECMO are scarce. This study analyzes the incidence and predictors of VTE in patients treated with ECMO due to respiratory failure. METHODS: Retrospective analysis of patients treated on ECMO in our center from 04/2010 to 11/2015. Patients with thromboembolic events prior to admission were excluded. Diagnosis was made by imaging in survivors and postmortem examination in deceased patients. RESULTS: Out of 102 screened cases, 42 survivors and 21 autopsy cases [mean age 46.0 ± 14.4 years; 37 (58.7 %) males] fulfilling the above-mentioned criteria were included. Thirty-four patients (54.0 %) underwent ECMO therapy due to ARDS, and 29 patients (46.0 %) with chronic organ failure were bridged to lung transplantation. Despite systemic anticoagulation at a mean PTT of 50.6 ± 12.8 s, [VT/VTE 47.0 ± 12.3 s and no VT/VTE 53.63 ± 12.51 s (p = 0.037)], VT and/or VTE was observed in 29 cases (46.1 %). The rate of V. cava thrombosis was 15/29 (51.7 %). Diagnosis of pulmonary embolism prevailed in deceased patients [5/21 (23.8 %) vs. 2/42 (4.8 %) (p = 0.036)]. In a multivariable analysis, only aPTT and time on ECMO predicted VT/VTE. There was no difference in the incidence of clinically diagnosed VT in ECMO survivors and autopsy findings. CONCLUSIONS: Venous thrombosis and thromboembolism following ECMO therapy are frequent. Quality of anticoagulation and ECMO runtime predicted thromboembolic events

“Awake” extracorporeal membrane oxygenation (ECMO): pathophysiology, technical considerations, and clinical pioneering

Venovenous extracorporeal membrane oxygenation (vv-ECMO) has been classically employed as a rescue therapy for patients with respiratory failure not treatable with conventional mechanical ventilation alone. In recent years, however, the timing of ECMO initiation has been readdressed and ECMO is often started earlier in the time course of respiratory failure. Furthermore, some centers are starting to use ECMO as a first line of treatment, i.e., as an alternative to invasive mechanical ventilation in awake, non-intubated, spontaneously breathing patients with respiratory failure ("awake" ECMO). There is a strong rationale for this type of respiratory support as it avoids several side effects related to sedation, intubation, and mechanical ventilation. However, the complexity of the patient-ECMO interactions, the difficulties related to respiratory monitoring, and the management of an awake patient on extracorporeal support together pose a major challenge for the intensive care unit staff. Here, we review the use of vv-ECMO in awake, spontaneously breathing patients with respiratory failure, highlighting the pros and cons of this approach, analyzing the pathophysiology of patient-ECMO interactions, detailing some of the technical aspects, and summarizing the initial clinical experience gained over the past years

Nurses' perceptions of aids and obstacles to the provision of optimal end of life care in ICU

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Arterial elastance and heart-arterial coupling in aortic regurgitation are determined by aortic leak severity

Background In aortic valve regurgitation (AR), aortic leak severity modulates left ventricle (LV) arterial system interaction. The aim of this study was to assess (1) how arterial elastance (E-a), calculated as the ratio of LV end-systolic pressure and stroke volume, relates to arterial properties and leak severity and (2) the validity of E-a/E-max (with E-max the slope of the-end-systolic pressure-volume relation) as a heart-arterial coupling parameter in AR. Methods and Results Our work is based on human data obtained from a study on vascular adaptation in chronic AR. These data allowed us to assess the parameters of a computer model of heart-arterial interaction. In particular, total peripheral resistance (R) and aortic leak severity-expressed as leak resistance (R-L,R-ao)-were quantified for different patient subgroups (group I/IIa/IIb: E-max = 2.15/0.62/0.47 mm Hg/mL; E-a = 1.24/0.66/0.90 mm Hg/mL; R = 1.9/0.6/0.85 mm Hg-s/mL, R-L,R-ao = 0.35/0.05/0.20 mm Hg-s/mL). A parameter study demonstrated that R-L,R-ao was the main determinant of E-a. With all other parameters constant, valve repair would increase E-a to 2.81, 1.08, and 1.54 mm Hg/mL in groups I,IIa, and IIb, respectively. For a given E-a/E-max, LV pump efficiency (estimated as the ratio of stroke work and LV systolic pressure-volume area) was lower than the theoretical predicted value, except for the simulations with intact aortic valve. Conclusions In AR(a) E-a is determined by aortic leak severity rather than by arterial system properties. Using E-a/E-max as a coupling parameter in general or as a mechanico-energetic regulatory parameter in particular is questionable

Early detection of abnormal left ventricular relaxation in acute myocardial ischemia with a quadratic model

Aims: The time constant of left ventricular (LV) relaxation derived from a monoexponential model is widely 12 used as an index of LV relaxation rate, although this model does not reflect the non-uniformity of ventricular 13 relaxation. This study investigates whether the relaxation curve can be better fitted with a “quadratic” model 14 than with the “conventional” monoexponential model and if changes in the LV relaxation waveform due to 15 acute myocardial ischemia could be better detected with the quadratic model. 16 Methods and results: Isovolumic relaxation was assessed with quadratic and conventional models during acute 17 myocardial ischemia performed in 6 anesthetized pigs. Mathematical development indicates that one parameter 18 (Tq) of the quadratic model reflects the rate of LV relaxation, while the second parameter (K) modifies the 19 shape of the relaxation curve. Analysis of experimental data obtained in anesthetized pigs showed that the shape 20 of LV relaxation consistently deviates from the conventional monoexponential decay. During the early phase of 21 acute myocardial ischemia, the rate and non-uniformity of LV relaxation, assessed with the quadratic function, 22 were significantly enhanced. Tq increased by 16% (p < 0.001) and K increased by 12% (p < 0.001) within 30 23 and 60 minutes, respectively, after left anterior descending (LAD) coronary artery occlusion. However, no 24 significant changes were observed with the conventional monoexponential decay within 60 minutes of ischemia. 25 Conclusions: The quadratic model better fits LV isovolumic relaxation than the monoexponential model and can 26 detect early changes in relaxation due to acute myocardial ischemia that are not detectable with conventional 27 methods

Effect of a novel thromboxane A(2) inhibitor on right ventricular-arterial coupling in endotoxic shock

We investigated the effects of a dual thromboxane (TX)A(2) synthase inhibitor and TXA(2) receptor antagonist (BM-573) on right ventricular-arterial coupling in a porcine model of endotoxic shock. Thirty minutes before the onset of 0.5 mg/kg endotoxin infusion, six pigs (Endo group) received an infusion with a placebo solution, and six other pigs (Anta group) with BM-573. Right ventricular pressure-volume loops were obtained by the conductance catheter technique. The slope (E-es) of the end-systolic pressure-volume relationship and its volume intercept at 25 mmHg were calculated as measures of right ventricular systolic function. RV afterload was quantified by pulmonary arterial elastance (E-a), and E-es/E-a ratio represented right ventricular-arterial coupling. Mechanical efficiency was defined as the ratio of stroke work and pressure-volume area. In this model of endotoxic shock, BM-573 blunted the early phase of pulmonary hypertension, improved arterial oxygenation, and prevented a decrease in right ventricular myocardial efficiency and right ventricular dilatation. However, the drug could not prevent the loss of homeometric regulation and alterations in right ventricular-arterial coupling. In conclusion, dual TXA(2) synthase inhibitor and receptor antagonists such as BM-573 have potential therapeutic applications, improving right ventricular efficiency and arterial oxygenation in endotoxic shock

Effects of endotoxic shock on right ventricular systolic function and mechanical efficiency

Objective: To investigate the effects of endotoxin infusion on right ventricular (RV) systolic function and mechanical efficiency. Methods: Six anesthetized pigs (Endo group) received a 0.5 mg/kg endotoxin infusion over 30 min and were compared with six other anesthetized pigs (Control group) receiving placebo for 5 h. RV pressure-volume (PV) loops were obtained by the conductance catheter technique and pulmonary artery flow and pressure were measured with high-fidelity transducers. Results: RV adaptation to increased afterload during the early phase of endotoxin-induced pulmonary hypertension (T30) was obtained by both homeometric and hetereometric regulations: the slope of the end-systolic PV relationship of the right ventricle increased from 1.4+/-0.2 mmHg/ml to 2.9+/-0.4 mmHg/ml (P<0.05) and RV end-diastolic volume increased from 56+/-6 ml to 64+/-11 ml (P<0.05). Consequently, right ventricular-vascular coupling was maintained at a maximum efficiency. Ninety minutes later (T120), facing the same increased afterload, the right ventricle failed to maintain its contractility to such an elevated level and, as a consequence, right ventricular-vascular uncoupling occurred. PV loop area, which is known to be highly correlated with oxygen myocardial consumption, increased from 1154+/-127 mmHg/ml (T0) to 1798+/-122 mmHg/ml (T180) (P<0.05) while RV mechanical efficiency decreased from 63+/-2% (T0) to 45+/-5% (T270) (P<0.05). Conclusions: In the very early phase of endotoxinic shock, right ventricular-vascular coupling is preserved by an increase in RV contractility. Later, myocardial oxygen consumption and energetic cost of RV contractility are increased, as evidenced by the decrease in RV efficiency, and right ventricular-vascular uncoupling occurs. Therefore, therapies aiming at restoring right ventricular-vascular coupling in endotoxic shock should attempt to increase RV contractility and to decrease RV afterload but also to preserve RV mechanical efficiency. (C) 2003 European Society of Cardiology. Published by Elsevier B.V. All rights reserved