Search

Background: Multiple major health organisations recommend the use of extracorporeal membrane oxygenation (ECMO) support for COVID-19-related acute hypoxaemic respiratory failure. However, initial reports of ECMO use in patients with COVID-19 described very high mortality and there have been no large, international cohort studies of ECMO for COVID-19 reported to date. Methods: We used data from the Extracorporeal Life Support Organization (ELSO) Registry to characterise the epidemiology, hospital course, and outcomes of patients aged 16 years or older with confirmed COVID-19 who had ECMO support initiated between Jan 16 and May 1, 2020, at 213 hospitals in 36 countries. The primary outcome was in-hospital death in a time-to-event analysis assessed at 90 days after ECMO initiation. We applied a multivariable Cox model to examine whether patient and hospital factors were associated with in-hospital mortality. Findings: Data for 1035 patients with COVID-19 who received ECMO support were included in this study. Of these, 67 (6%) remained hospitalised, 311 (30%) were discharged home or to an acute rehabilitation centre, 101 (10%) were discharged to a long-term acute care centre or unspecified location, 176 (17%) were discharged to another hospital, and 380 (37%) died. The estimated cumulative incidence of in-hospital mortality 90 days after the initiation of ECMO was 37·4% (95% CI 34·4–40·4). Mortality was 39% (380 of 968) in patients with a final disposition of death or hospital discharge. The use of ECMO for circulatory support was independently associated with higher in-hospital mortality (hazard ratio 1·89, 95% CI 1·20–2·97). In the subset of patients with COVID-19 receiving respiratory (venovenous) ECMO and characterised as having acute respiratory distress syndrome, the estimated cumulative incidence of in-hospital mortality 90 days after the initiation of ECMO was 38·0% (95% CI 34·6–41·5). Interpretation: In patients with COVID-19 who received ECMO, both estimated mortality 90 days after ECMO and mortality in those with a final disposition of death or discharge were less than 40%. These data from 213 hospitals worldwide provide a generalisable estimate of ECMO mortality in the setting of COVID-19. Funding: None.

A 27-year-old man, with a history of renal transplantation, presented with acute kidney failure andPneumocystis jiroveciipneumonia. The patient developed severe acute respiratory failure and required support by veno-venous extracorporeal membrane oxygenation for a total of 59 days. During this period, the patient had extremely low tidal volumes using a lung protective ventilation strategy and intermittent prone positioning was used to optimise oxygenation. There was full recovery of pulmonary and partial recovery of renal function.

Study objective: The mini-fluid challenge may predict fluid responsiveness with minimum risk of fluid overloading. However, the amount of fluid as well as the best manner to evaluate the effect is unclear. In this prospective observational pilot study, the value of changes in pulse contour cardiac output (CO) measurements during mini-fluid challenges is investigated. Design: Prospective observational study. Setting: Intensive Care Unit of a university hospital. Patients: Twenty-one patients directly after elective cardiac surgery on mechanical ventilation. Interventions: The patients were subsequently given 10 intravenous boluses of 50 mL of hydroxyethyl starch with a total of 500 mL per patient while measuring pulse contour CO. Measurements: We measured CO by minimal invasive ModelflowR (COm) and PulseCOR (COli), before and one minute after each fluid bolus. We analyzed the smallest volume that was predictive of fluid responsiveness. A positive fluid response was defined as an increase in CO of > 10% after 500 mL fluid infusion. Main results: Fifteen patients (71%) were COm responders and 13 patients (62%) COli responders. An increase in COm after 150 mL of fluid > 5.0% yielded a positive and negative predictive value (+ PV and − PV) of 100% with an area under the curve (AUC) of 1.00 (P < 0.001). An increase in COli > 6.3% after 200 mL was able to predict a fluid response in COli after 500 mL with a + PV of 100% and − PV of 73%, with an AUC of 0.88 (P < 0.001). Conclusion: The use of minimal invasive ModelflowR pulse contour CO measurements following a mini-fluid challenge of 150 mL can predict fluid responsiveness and may help to improve fluid management.

Objective: We studied the variable effects of norepinephrine infusion on cardiac output in postoperative cardiac surgical patients in whom norepinephrine increased mean arterial pressure. We hypothesized that the directional change in cardiac output would be determined by baseline cardiac function, as quantified by stroke volume variation, and the subsequent changes in mean systemic filling pressure and vasomotor tone. Design: Intervention study. Setting: ICU of a university hospital. Patients: Sixteen mechanically ventilated postoperative cardiac surgery patients. Interventions: Inspiratory holds were performed at baseline-1, during increased norepinephrine infusion, and baseline-2 conditions. Measurements and Main Results: We measured mean arterial pressure, heart rate, central venous pressure, cardiac output, stroke volume variation and, with use of inspiratory hold maneuvers, mean systemic filling pressure, then calculated re sistance for venous return and systemic vascular resistance. Increasing norepinephrine by 0.04 ± 0.02 μg·kg -1 ·min -1 increased mean arterial pressure 20 mm Hg in all patients. Cardiac output decreased in ten and increased in six patients. In all patients mean systemic filling pressure, systemic vascular resistance and resistance for venous return increased and stroke volume variation decreased. Resistance for venous return and systemic vascular resistance increased more (p = 0.019 and p = 0.002) in the patients with a cardiac output decrease. Heart rate decreased in the patients with a cardiac output decrease (p = 0.002) and was unchanged in the patients with a cardiac output increase. Baseline stroke volume variation was higher in those in whom cardiac output increased (14.4 ± 4.2% vs. 9.1 ± 2.4%, p = 0.012). Stroke volume variation >8.7% predicted the increase in cardiac output to norepinephrine (area under the receiver operating characteristic curve 0.900). Conclusions: The change in cardiac output induced by norepinephrine is determined by the balance of volume recruitment (increase in mean systemic filling pressure), change in resistance for venous return, and baseline heart function. Furthermore, the response of cardiac output on norepinephrine can be predicted by baseline stroke volume variation. (Crit Care Med 2013; 41:143–150)

Purpose To assess the level of agreement between different bedside estimates of effective circulating blood volume—mean systemic filling pressure (Pmsf), arm equilibrium pressure (Parm) and model analog (Pmsa)—in ICU patients. Methods Eleven mechanically ventilated postoperative cardiac surgery patients were studied. Sequential measures were made in the supine position, rotating the bed to a 30° head-up tilt and after fluid loading (500 ml colloid). During each condition four inspiratory hold maneuvers were done to determine Pmsf; arm stop-flow was created by inflating a cuff around the upper arm for 30 s to measure Parm, and Pmsa was estimated from a Guytonian model of the systemic circulation. Results Mean Pmsf, Parm and Pmsa across all three states were 20.9 ± 5.6, 19.8 ± 5.7 and 14.9 ± 4.0 mmHg, respectively. Bland-Altman analysis for the difference between Parm and Pmsf showed a non-significant bias of −1.0 ± 3.08 mmHg (p = 0.062), a coefficient of variation (COV) of 15 %, and limits of agreement (LOA) of −7.3 and 5.2 mmHg. For the difference between Pmsf and Pmsa we found a bias of −6.0 ± 3.1 mmHg (p

BACKGROUND: Mean systemic filling pressure (Pmsf) can be determined at the bedside by measuring central venous pressure (Pcv) and cardiac output (CO) during inspiratory hold maneuvers. Critical closing pressure (Pcc) can be determined using the same method measuring arterial pressure (Pa) and CO. If Pcc > Pmsf, there is then a vascular waterfall. In this study, we assessed the existence of a waterfall and its implications for the calculation of vascular resistances by determining Pmsf and Pcc at the bedside. METHODS: In 10 mechanically ventilated postcardiac surgery patients, inspiratory hold maneuvers were performed, transiently increasing Pcv and decreasing Pa and CO to 4 different steady-state levels. For each patient, values of Pcv and CO were plotted in a venous return curve to determine Pmsf. Similarly, Pcc was determined with a ventricular output curve plotted for Pa and CO. Measurements were performed in each patient before and after volume expansion with 0.5 L colloid, and vascular resistances were calculated. RESULTS: For every patient, the relationship between the 4 measurements of Pcv and CO and of Pa and CO was linear. Baseline Pmsf was 18.7 ± 4.0 mm Hg (mean ± SD) and differed significantly from Pcc 45.5 ± 11.1 mm Hg (P < 0.0001). The difference of Pcc and Pmsf was 26.8 ± 10.7 mm Hg, indicating the presence of a systemic vascular waterfall. Volume expansion increased Pmsf (26.3 ± 3.2 mm Hg), Pcc (51.5 ± 9.0 mm Hg), and CO (5.5 ± 1.8 to 6.8 ± 1.8 L · min). Arterial (upstream of Pcc) and venous (downstream of Pmsf) vascular resistance were 8.27 ± 4.45 and 2.75 ± 1.23 mm Hg · min · L; the sum of both (11.01 mm Hg · min · L) was significantly different from total systemic vascular resistance (16.56 ± 8.57 mm Hg · min · L; P = 0.005). Arterial resistance was related to total resistance. CONCLUSIONS: Vascular pressure gradients in cardiac surgery patients suggest the presence of a vascular waterfall phenomenon, which is not affected by CO. Thus, measures of total systemic vascular resistance may become irrelevant in assessing systemic vasomotor tone. Copyright © 2012 International Anesthesia Research Society.

Mean systemic filling pressure (Pmsf) can be measured at the bedside with minimally invasive monitoring in ventilator-dependent patients using inspiratory hold maneuvers (Pmsf(hold)) as the zero flow intercept of cardiac output (CO) to central venous pressure (CVP) relation. We compared Pmsf(hold) with arm vascular equilibrium pressure during vascular occlusion (Pmsf(arm)) and their ability to assess systemic vascular compliance (Csys) and stressed volume by intravascular fluid administration.In mechanically ventilated postoperative cardiac surgery patients, inspiratory holds at varying airway pressures and arm stop-flow maneuvers were performed during normovolemia and after each of 10 sequential 50-mL bolus colloid infusions. We measured CVP, Pmsf(arm), stroke volume, and CO during fluid administration steps to construct CVP to CO (cardiac function) curves and Δvolume/ΔPmsf (compliance) curves. Pmsf(hold) was measured before and after fluid administration. Stressed volume was determined by extrapolating the Pmsf-volume curve to zero pressure intercept.Fifteen patients were included. Pmsf(hold) and Pmsf(arm) were closely correlated. Csys was linear (64.3 ± 32.7 mL · mm Hg(-1), 0.97 ± 0.49 mL · mm Hg(-1) · kg(-1) predicted body weight). Stressed volume was estimated to be 1265 ± 541 mL (28.5% ± 15% predicted total blood volume). Cardiac function curves of patients with an increase of12% to 500 mL volume extension (volume responsive) were steep, whereas the cardiac function curves of the remaining patients were flat.Csys, stressed volume, and cardiac function curves can be determined at the bedside and can be used to characterize patients' hemodynamic status.

Background and objective In pharmacological research, arm occlusion pressure is used to study haemodynamic effects of drugs. However, arm occlusion pressure might be an indicator of static filling pressure of the arm. We hypothesised that arm occlusion pressure can be used to predict fluid loading responsiveness. Methods Twenty-four patients who underwent cardiac surgery were studied during their first 2 h in the ICU. The lungs were ventilated mechanically and left ventricular function was supported as necessary. Arm occlusion pressure was defined as the radial artery pressure after occluding arterial flow for 35 s by a blood pressure cuff inflated to 50mmHg above SBP. The cuff was positioned around the arm in which a radial artery catheter had been inserted. Measurements were performed before (baseline) and after fluid loading (500 ml hydroxyethyl starch 6%). Patients whose cardiac output increased by at least 10% were defined as responders. Results In responders (n=17), arm occlusion pressure, mean arterial pressure and central venous pressure increased and stroke volume variation and pulse pressure variation decreased. In non-responders (n=7), arm occlusion pressure and central venous pressure increased, and pulse pressure variation decreased. Mean arterial pressure, stroke volume variation and heart rate did not change significantly. The area under the curve to predict fluid loading responsiveness for arm occlusion pressure was 0.786 (95% confidence interval 0.567-1.000), at a cut-off of 21.9 mmHg, with sensitivity of 71% and specificity of 88% in predicting fluid loading responsiveness. Prediction of responders with baseline arm occlusion pressure was as good as baseline stroke volume variation and pulse pressure variation. Conclusion Arm occlusion pressure was a good predictor of fluid loading responsiveness in our group of cardiac surgery patients and offers clinical advantages over stroke volume variation and pulse pressure variation. © 2011 Copyright European Society of Anaesthesiology.

The volemic status of a patient can be determined by measuring mean systemic filling pressure (Pmsf). Pmsf is obtained from the venous return curve, i.e. the relationship between central venous pressure (Pcv) and blood flow. We evaluated the feasibility and precision of Pmsf measurement. In ten piglets we constructed venous return curves using seven 12 s inspiratory holds transiently increasing Pcv to seven different steady state levels and monitored the resultant blood flow, by pulse contour (COpc) and by flow probes around the pulmonary artery (COr) and aorta (COl). Pmsf is obtained by extrapolation of the venous return curve to zero flow. Measurements were repeated to evaluate the precision of Pmsf. During the inspiratory holds, 133 paired data points were obtained for COr, COl, COpc and Pcv. Bland–Altman analysis showed no difference between COr and COl, but a small significant difference was present between COl and COpc. All Pcv versus flow (COl or COpc) relationships were linear. Mean Pmsf was 10.78 with COl and 10.37 mmHg with COpc. Bland–Altman analysis for Pmsf with COl and with COpc, showed a bias of 0.40 ± 0.48 mmHg. The averaged coefficient of variation for repeated measurement of Pmsf with COl was 6.2% and with COpc 6.1%. During an inspiratory hold pulmonary flow and aortic flow equilibrate. Cardiac output estimates by arterial pulse contour and by a flow probe around the aorta are interchangeable. Therefore, the venous return curve and Pmsf can be estimated accurately by pulse contour methods.

OBJECTIVE We present a new physiological model that discriminated between changes in the systemic arterial and venous circulation. To test our model, we studied the effects of dobutamine and hypovolemia in intact pentabarbital-anesthetized piglets. METHODS Aorta pressure (Pao), central venous pressure (Pcv), mean systemic filling pressure (Pmsf) and cardiac output (CO), were measured in 10 piglets, before, during and after dobutamine infusion (6 µg kg⁻¹ min⁻¹), as well as during hypovolemia (-10 mL kg⁻¹), and after fluid resuscitation to normovolemia. Venous (Rv) and total systemic (Rsys) resistance were determined from Pao, Pcv, Pmsf and CO. The quotient of Rv/Rsys was used to determine the predominant location of vascular changes (i.e. vasoconstriction or dilatation on either venous or arterial side). RESULTS Administration of dobutamine increased heart rate and CO, whereas it decreased Pmsf, Rsys, Rv and Rv/Rsys. The decrease in Rv was significantly greater than Rsys. Pao and Pcv did not change. Hypovolemia decreased CO, Pcv, Pmsf, Rv and Rv/Rsys, but kept Rsys constant and increased heart rate. CONCLUSIONS Hypovolemia and dobutamine differentially alter Pmsf, Rsys, Rv and Rv/Rsys ratio. The increase in CO during dobutamine infusion was attributed to the combined increased cardiac function and decreased Rv. The decrease in CO with hypovolemia was due to a decreased Pmsf but was partly compensated for by a decrease in Rv tending to preserve venous return and thus CO.

The physiology of the venous part of the human circulation seems to be a forgotten component of the circulation in critical care medicine. One of the main reasons, probably, is that measures of right atrial pressure (Pra) do not seem to be directly linked to blood flow. This perception is primarily due to an inability to measure the pressure gradient for venous return. The upstream pressure for venous return is mean systemic filling pressure (Pmsf) and it does not lend itself easily to be measured. Recent clinical studies now demonstrate the basic principles underpinning the measure of Pmsf at the bedside.Using routinely available minimally invasive monitoring of continuous cardiac output and Pra, one can accurately construct venous return curves by performing a series of end-inspiratory hold maneuvers, in ventilator-dependent patients. From these venous return curves, the clinician can now finally obtain at the bedside not only Pmsf but also the derived parameters: resistance to venous return, systemic compliance and stressed volume.Measurement of Pmsf is essential to describe the control of vascular capacitance. It is the key to distinguish between passive and active mechanisms of blood volume redistribution and partitioning total blood volume in stressed and unstressed volume.

OBJECTIVE:: To measure the relationship between blood flow and central venous pressure (Pcv) and to estimate mean systemic filling pressure (Pmsf), circulatory compliance, and stressed volume in patients in the intensive care unit. DESIGN:: Intervention study. SETTING:: Intensive care unit of a university hospital. PATIENTS:: Twelve mechanically ventilated postoperative cardiac surgery patients. INTERVENTIONS:: Inspiratory holds were performed during normovolemia in supine position (baseline), relative hypovolemia by placing the patients in 30 degree head-up position (hypo), and relative hypervolemia by volume loading with 0.5 L colloid (hyper). MEASUREMENTS AND MAIN RESULTS:: We measured the relationship between blood flow and Pcv using 12-second inspiratory-hold maneuvers transiently increasing Pcv to three different steady-state levels and monitored the resultant blood flow via the pulse contour method during the last 3 seconds. The Pcv to blood flow relation was linear for all measurements with a slope unaltered by relative volume status. Pmsf decreased with hypo and increased with hyper (18.8 ± 4.5 mm Hg, to 14.5 ± 3.0 mm Hg, to 29.1 ± 5.2 mm Hg [baseline, hypo, hyper, respectively, p < 0.05]). Baseline total circulatory compliance was 0.98 mL•mm Hg•kg and stressed volume was 1677 mL. CONCLUSIONS:: Pmsf can be determined in intensive care patients with an intact circulation with use of inspiratory pause procedures, making serial measures of circulatory compliance and circulatory stressed volume feasible. © 2009 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.

A best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was whether the administration of amiodarone or lidocaine in patients with refractory VT/VF after cardiac surgery results in successful cardioversion. Altogether more than 434 papers were found using the reported search, from which 23 articles were used to answer the clinical question. No randomized trials have been found in which amiodarone was studied in patients with refractory VF/VT after cardiac surgery. Recommendations on the use of amiodarone in patients with refractory VF/VT in both European and American 2005 Guidelines on Resuscitation are mainly based on expert consensus and are supported by a few randomized trials in patients with out-of-hospital cardiac arrest. We would therefore recommend that amiodarone is the first line drug that should be used in patients with refractory ventricular arrhythmias after cardiac surgery that persist after three failed attempts at cardioversion. Lidocaine should only be used if amiodarone is not available or if its use is contraindicated. Amiodarone should be administered as an intravenous bolus of 300 mg after the third unsuccessful shock.

Objective:Tranexamic acid has beensuggestedto be as effectiveas aprotininin reducingbloodloss andtransfusionrequirements after cardiac surgery. Previous studies directly comparing both antifibrinolytics focus on high-risk cardiac surgery patients only or suffer from methodological problems. We wanted to compare the effectiveness of tranexamic acid versus aprotinin in reducing postoperative blood loss and transfusion requirements in the patient group representing the majority of cardiac surgery patients: low- and intermediate-risk patients. Methods: We conducted a non-sponsored, double-blind, randomised, placebo-controlled trial in which 298 patients scheduled for low- or intermediate-risk (mean logistic EuroSCORE 4.1) first-time heart surgery with use of cardiopulmonary bypass were randomised to receive either tranexamic acid, high-dose aprotinin, or placebo. All patients had preoperative normal renal function. End points of the study were monitored from the time of surgeryuntil patientdischarge.Thistrial wasexecutedbetweenJune 2004andOctober2006.Results:Both antifibrinolytics significantly reduced bloodloss andtransfusionrequirements when comparedwith placebo.Aprotininwas abouttwice aseffective as tranexamic acidin reducingtotal postoperative blood loss (estimated median difference 155 ml, 95% confidence interval (CI) 60—260; p < 0.001). Accordingly, aprotinin reduced packed red blood cell transfusions more than tranexamic acid, although the difference did not reach statistical significance. Only aprotinin significantly reduced the proportion of transfused patients when compared with placebo (mean difference � 20.9%, 95% CI 7.3—33.5; p = 0.013), and only aprotinin completely abolished bleeding-related re-explorations (mean difference 6.8%, 95% CI 1.6—13.4%; p = 0.004). Neither antifibrinolytic agent increased the incidence of mortality (mean difference tranexamic acid � 0.4%, 95% CI � 4.6 to 4.4; p = 0.79, mean differenceaprotinin � 1.3%, 95% CI � 6.2 to 3.5;p = 0.62) or other seriousadverse events when comparedwith placebo.Conclusion:Aprotinin has clinically significant advantages over tranexamic acid in patients with normal renal function scheduled for low- or intermediate-risk cardiac surgery.

Guyton's theory on venous return, implying a linear relationship between blood flow and central venous pressure, was tested in 12 mechanically ventilated ICU patients during standard care.