Determination of cardiac output from pulse pressure contour during intra-aortic balloon pumping in patients with low ejection fraction.

Evaluation of a new Windkessel model based pulse contour method (WKflow) to calculate stroke volume in patients undergoing intra-aortic balloon pumping (IABP). Preload changes were induced by vena cava occlusions (VCO) in twelve patients undergoing cardiac surgery to vary stroke volume (SV), which was measured by left ventricular conductance volume method (SVlv) and WKflow (SVwf). Twelve VCO series were carried out during IABP assist at a 1:2 ratio and seven VCO series were performed with IABP switched off. Additionally, SVwf was evaluated during nine episodes of severe arrhythmia. VCO's produced marked changes in SV over 10-20 beats. 198 paired data sets of SVlv and SVwf were obtained. Bland-Altman analysis for the difference between SVlv and SVwf during IABP in 1:2 mode showed a bias (accuracy) of 1.04 ± 3.99 ml, precision 10.9% and limits of agreement (LOA) of - 6.94 to 9.02 ml. Without IABP bias was 0.48 ± 4.36 ml, precision 11.6% and LOA of - 8.24 to 9.20 ml. After one thermodilution calibration of SVwf per patient, during IABP the accuracy improved to 0.14 ± 3.07 ml, precision to 8.3% and LOA to - 6.00 to + 6.28 ml. Without IABP the accuracy improved to 0.01 ± 2.71 ml, precision to 7.5% and LOA to - 5.41 to + 5.43 ml. Changes in SVlv and SVwf were directionally concordant in response to VCO's and during severe arrhythmia. (R2 = 0.868). The SVwf and SVlv methods are interchangeable with respect to measuring absolute stroke volume as well as tracking changes in stroke volume. The precision of the non-calibrated WKflow method is about 10% which improved to 7.5% after one calibration per patient.

Cardiac output response to norepinephrine in postoperative cardiac surgery patients: interpretation with venous return and cardiac function curves.

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 resistance for venous return and systemic vascular resistance. Increasing norepinephrine by 0.04 ± 0.02 µg·kg·min 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.

Comparing hemodynamic effects with three different measurement devices, of two methods of external leg compression versus passive leg raising in patients after cardiac surgery.

External leg compression (ELC) may increase cardiac output (CO) in fluid-responsive patients like passive leg raising (PLR). We compared the hemodynamic effects of two methods of ELC and PLR measured by thermodilution (COtd), pressure curve analysis Modelflow™ (COmf) and ultra-sound HemoSonic™ (COhs), to evaluate the method with the greatest hemodynamic effect and the most accurate less invasive method to measure that effect. We compared hemodynamic effects of two different ELC methods (circular, A (n = 16), vs. wide, B (n = 13), bandages inflated to 30 cm H2O for 15 min) with PLR prior to each ELC method, in 29 post-operative cardiac surgical patients. Hemodynamic responses were measured with COtd, COmf and COhs. PLR A increased COtd from 6.1 ± 1.7 to 6.3 ± 1.8 L·min(-1) (P = 0.016), and increased COhs from 4.9 ± 1.5 to 5.3 ± 1.6 L·min(-1) (P = 0.001), but did not increase COmf. ELC A increased COtd from 6.4 ± 1.8 to 6.7 ± 1.9 L·min(-1) (P = 0.001) and COmf from 6.9 ± 1.7 to 7.1 ± 1.8 L·min(-1) (P = 0.021), but did not increase COhs. ELC A increased COtd and COmf as in PLR A. PLR B increased COtd from 5.4 ± 1.3 to 5.8 ± 1.4 L·min(-1) (P < 0.001), and COhs from 5.0 ± 1.0 to 5.4 ± 1.0 L·min(-1) (P = 0.013), but not COmf. ELC B increased COtd from 5.2 ± 1.2 to 5.4 ± 1.1 L·min(-1) (P = 0.003), but less than during PLR B (P = 0.012), while COmf and COhs did not change. Bland-Altman and polar plots showed lower limits of agreement with changes in COtd for COmf than for COhs. The circular leg compression increases CO more than bandage compression, and is able to increase CO as in PLR. The less invasive Modelflow™ can detect these changes reasonably well.

Determination of vascular waterfall phenomenon by bedside measurement of mean systemic filling pressure and critical closing pressure in the intensive care unit.

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(-1)). 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(-1); the sum of both (11.01 mm Hg · min · L(-1)) was significantly different from total systemic vascular resistance (16.56 ± 8.57 mm Hg · min · L(-1); 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.

Bedside assessment of total systemic vascular compliance, stressed volume, and cardiac function curves in intensive care unit patients.

BACKGROUND: 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. METHODS: 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. RESULTS: 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 of >12% to 500 mL volume extension (volume responsive) were steep, whereas the cardiac function curves of the remaining patients were flat. CONCLUSIONS: Csys, stressed volume, and cardiac function curves can be determined at the bedside and can be used to characterize patients' hemodynamic status.

Feasibility to estimate mean systemic filling pressure with inspiratory holds at the bedside.

Background: A decade ago, it became possible to derive mean systemic filling pressure (MSFP) at the bedside using the inspiratory hold maneuver. MSFP has the potential to help guide hemodynamic care, but the estimation is not yet implemented in common clinical practice. In this study, we assessed the ability of MSFP, vascular compliance (Csys), and stressed volume (Vs) to track fluid boluses. Second, we assessed the feasibility of implementation of MSFP in the intensive care unit (ICU). Exploratory, a potential difference in MSFP response between colloids and crystalloids was assessed. Methods: This was a prospective cohort study in adult patients admitted to the ICU after cardiac surgery. The MSFP was determined using 3-4 inspiratory holds with incremental pressures (maximum 35 cm H2O) to construct a venous return curve. Two fluid boluses were administered: 100 and 500 ml, enabling to calculate Vs and Csys. Patients were randomized to crystalloid or colloid fluid administration. Trained ICU consultants acted as study supervisors, and protocol deviations were recorded. Results: A total of 20 patients completed the trial. MSFP was able to track the 500 ml bolus (p < 0.001). In 16 patients (80%), Vs and Csys could be determined. Vs had a median of 2029 ml (IQR 1605-3164), and Csys had a median of 73 ml mmHg-1 (IQR 56-133). A difference in response between crystalloids and colloids was present for the 100 ml fluid bolus (p = 0.019) and in a post hoc analysis, also for the 500 ml bolus (p = 0.010). Conclusion: MSFP can be measured at the bedside and provides insights into the hemodynamic status of a patient that are currently missing. The clinical feasibility of Vs and Csys was judged ambiguously based on the lack of required hemodynamic stability. Future studies should address the clinical obstacles found in this study, and less-invasive alternatives to determine MSFP should be further explored. Clinical Trial Registration: ClinicalTrials.gov Identifier NCT03139929.

Methods in pharmacology: measurement of cardiac output.

Many methods of cardiac output measurement have been developed, but the number of methods useful for human pharmacological studies is limited. The 'holy grail' for the measurement of cardiac output would be a method that is accurate, precise, operator independent, fast responding, non-invasive, continuous, easy to use, cheap and safe. This method does not exist today. In this review on cardiac output methods used in pharmacology, the Fick principle, indicator dilution techniques, arterial pulse contour analysis, ultrasound and bio-impedance are reviewed.

Arm occlusion pressure is a useful predictor of an increase in cardiac output after fluid loading following cardiac surgery.

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 50 mmHg 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.

Evaluation of mean systemic filling pressure from pulse contour cardiac output and central venous pressure.

OBJECTIVE: 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. METHODS: 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. RESULTS: 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%. CONCLUSIONS: 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.

Bedside assessment of mean systemic filling pressure.

PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: 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.

Partitioning the resistances along the vascular tree: effects of dobutamine and hypovolemia in piglets with an intact circulation.

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.

Defining human mean circulatory filling pressure in the intensive care unit.

Potentially, mean circulatory filling pressure (Pmcf) could aid hemodynamic management in patients admitted to the intensive care unit (ICU). However, data regarding the normal range for Pmcf do not exist challenging its clinical use. We aimed to define the range for Pmcf for ICU patients and also calculated in what percentage of cases equilibrium between arterial blood pressure (ABP) and central venous pressure (CVP) was reached. In patients in whom no equilibrium was reached, we corrected for arterial-to-venous compliance differences. Finally, we studied the influence of patient characteristics on Pmcf. We hypothesized fluid balance, the use of vasoactive medication, being on mechanical ventilation, and the level of positive end-expiratory pressure would be positively associated with Pmcf. We retrospectively studied a cohort of 311 patients that had cardiac arrest in ICU while having active recording of ABP and CVP 1 min after death. Median Pmcf was 15 mmHg [interquartile range (IQR) 12-18]. ABP and CVP reached an equilibrium state in 52% of the cases. Correction for arterial-to-venous compliances differences resulted in a maximum alteration of 1.3 mmHg in Pmcf. Fluid balance over the last 24 h, the use of vasoactive medication, and being on mechanical ventilation were associated with a higher Pmcf. Median Pmcf was 15 mmHg (IQR 12-18). When ABP remained higher than CVP, correction for arterial-to-venous compliance differences did not result in a clinically relevant alteration of Pmcf. Pmcf was affected by factors known to alter vasomotor tone and effective circulating blood volume.NEW & NOTEWORTHY In a cohort of 311 intensive care unit (ICU) patients, median mean circulatory filling pressure (Pmcf) measured after cardiac arrest was 15 mmHg (interquartile range 12-18). In 48% of cases, arterial blood pressure remained higher than central venous pressure, but correction for arterial-to-venous compliance differences did not result in clinically relevant alterations of Pmcf. Fluid balance, use of vasopressors or inotropes, and being on mechanical ventilation were associated with a higher Pmcf.

Assessment of venous return curve and mean systemic filling pressure in postoperative cardiac surgery patients.

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 x mm Hg x 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.

Assessing fluid responses after coronary surgery: role of mathematical coupling of global end-diastolic volume to cardiac output measured by transpulmonary thermodilution.

BACKGROUND: Mathematical coupling may explain in part why cardiac filling volumes obtained by transpulmonary thermodilution may better predict and monitor responses of cardiac output to fluid loading than pressures obtained by pulmonary artery catheters (PACs). METHODS: Eleven consecutive patients with hypovolaemia after coronary surgery and a PAC, allowing central venous pressure (CVP) and continuous cardiac index (CCIp) measurements, received a femoral artery catheter for transpulmonary thermodilution measurements of global end-diastolic blood volume index (GEDVI) and cardiac index (CItp). One to five colloid fluid-loading steps of 250 ml were done in each patient (n = 48 total). RESULTS: Fluid responses were predicted and monitored similarly by CItp and CCIp, whereas CItp and CCIp correlated at r = 0.70 (P < 0.001) with a bias of 0.40 l min(-1) m(-2). Changes in volumes (and not in CVP) related to changes in CItp and not in CCIp. Changes in CVP and GEDVI similarly related to changes in CItp, after exclusion of two patients with greatest CItp outliers (as compared to CCIp). Changes in GEDVI correlated better to changes in CItp when derived from the same thermodilution curve than to changes in CItp of unrelated curves and changes in CCIp. CONCLUSIONS: After coronary surgery, fluid responses can be similarly assessed by intermittent transpulmonary and continuous pulmonary thermodilution methods, in spite of overestimation of CCIp by CItp. Filling pressures are poor monitors of fluid responses and superiority of GEDVI can be caused, at least in part, by mathematical coupling when cardiac volume and output are derived from the same thermodilution curve.

A mini-fluid challenge of 150mL predicts fluid responsiveness using ModelflowR pulse contour cardiac output directly after cardiac surgery.

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 50mL of hydroxyethyl starch with a total of 500mL 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 500mL fluid infusion. MAIN RESULTS: Fifteen patients (71%) were COm responders and 13 patients (62%) COli responders. An increase in COm after 150mL 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 200mL was able to predict a fluid response in COli after 500mL 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 150mL can predict fluid responsiveness and may help to improve fluid management.

Estimating mean circulatory filling pressure in clinical practice: a systematic review comparing three bedside methods in the critically ill.

The bedside hemodynamic assessment of the critically ill remains challenging since blood volume, arterial-venous interaction and compliance are not measured directly. Mean circulatory filling pressure (Pmcf) is the blood pressure throughout the vascular system at zero flow. Animal studies have shown Pmcf provides information on vascular compliance, volume responsiveness and enables the calculation of stressed volume. It is now possible to measure Pmcf at the bedside. We performed a systematic review of the current Pmcf measurement techniques and compared their clinical applicability, precision, accuracy and limitations. A comprehensive search strategy was performed in PubMed, Embase and the Cochrane databases. Studies measuring Pmcf in heart-beating patients at the bedside were included. Data were extracted from the articles into predefined forms. Quality assessment was based on the Newcastle-Ottawa Scale for cohort studies. A total of 17 prospective cohort studies were included. Three techniques were described: Pmcf hold, based on inspiratory hold-derived venous return curves, Pmcf arm, based on arterial and venous pressure equilibration in the arm as a model for the entire circulation, and Pmcf analogue, based on a Guytonian mathematical model of the circulation. The included studies show Pmcf to accurately follow intravascular fluid administration and vascular compliance following drug-induced hemodynamic changes. Bedside Pmcf measures allow for more direct assessment of circulating blood volume, venous return and compliance. However, studies are needed to determine normative Pmcf values and their expected changes to therapies if they are to be used to guide clinical practice.

Hemodynamic effects of short-term hyperoxia after coronary artery bypass grafting.

BACKGROUND: Although oxygen is generally administered in a liberal manner in the perioperative setting, the effects of oxygen administration on dynamic cardiovascular parameters, filling status and cerebral perfusion have not been fully unraveled. Our aim was to study the acute hemodynamic and microcirculatory changes before, during and after arterial hyperoxia in mechanically ventilated patients after coronary artery bypass grafting (CABG) surgery. METHODS: This was a single-center physiological study in a tertiary care ICU in the Netherlands. Twenty-two patients scheduled for ICU admission after elective CABG were enrolled in the study between September 2014 and September 2015. In the ICU, patients were exposed to a fraction of inspired oxygen (FiO2) of 90% allowing a 15-min wash-in period. Various hemodynamic parameters were measured using direct pressure signals and continuous arterial waveform analysis at three sequential time points: before, during and after hyperoxia. RESULTS: During a 15-min exposure to a fraction of inspired oxygen (FiO2) of 90%, the partial pressure of arterial oxygen (PaO2) and arterial oxygen saturation (SaO2) were significantly higher. The systemic resistance increased (P < 0.0001), without altering the heart rate. Stroke volume variation and pulse pressure variation decreased slightly. The cardiac output did not significantly decrease (P = 0.08). Mean systemic filling pressure and arterial critical closing pressure increased (P < 0.01whereas the percentage of perfused microcirculatory vessels decreased (P < 0.01). Other microcirculatory parameters and cerebral blood flow velocity showed only slight changes. CONCLUSIONS: We found that short-term hyperoxia affects hemodynamics in ICU patients after CABG. This was translated in several changes in central circulatory variables, but had only slight effects on cardiac output, cerebral blood flow and the microcirculation. Clinical trial registration Netherlands Trial Register: NTR5064.

Breath-to-breath analysis of abdominal and rib cage motion in surfactant-depleted piglets during high-frequency oscillatory ventilation.

OBJECTIVE: To assess the value of monitoring abdominal and rib cage tidal displacement as an indicator of optimal mean airway pressure (Paw) during high-frequency oscillatory ventilation (HFOV). DESIGN AND SETTING: Prospective observational study in a university research laboratory. ANIMALS: Eight piglets weighing 12.0+/-0.5 kg, surfactant depleted by lung lavage. INTERVENTIONS: Compliance of the respiratory system (C(rs)) was calculated from a quasistatic pressure volume loop. After initiation of HFOV lung volume was recruited by increasing Paw to 40 cmH(2)O. Then mean Paw was decreased in steps until PaO(2)/FIO(2) was below 100 mmHg. Proximal pressure amplitude remained constant. MEASUREMENTS AND RESULTS: Abdominal and rib cage tidal displacement was determined using respiratory inductive plethysmography. During HFOV there was maximum in tidal volume (Vt) in seven of eight piglets. At maximal mean Paw abdominal and rib cage displacement were in phase. Phase difference between abdominal and rib cage displacement increased to a maximum of 178+/-28 degrees at minimum mean Paw. A minimum in abdominal displacement and a maximum of Vt was found near the optimal mean Paw, defined as the lowest mean Paw where shunt fraction is below 0.1. CONCLUSIONS: During HFOV abdominal and rib cage displacement displayed mean Paw dependent asynchrony. Maximal Vt and minimal abdominal displacement coincided with optimal C(rs), oxygenation, and ventilation, suggesting potential clinical relevance of monitoring Vt and abdominal displacement during HFOV.

Estimation of regional lung volume changes by electrical impedance pressures tomography during a pressure-volume maneuver.

OBJECTIVE: To assess the degree of linearity between lung volume and impedance change by electrical impedance tomography (EIT) in pigs with acute lung injury and to investigate regional impedance changes during a pressure-volume maneuver. DESIGN AND SETTING: Experimental animal study in a university research laboratory. PATIENTS AND PARTICIPANTS: Nine pigs with lung injury induced by lung lavage. INTERVENTIONS: The lungs were insufflated to four different lung volumes. Next the lungs were inflated in steps up to 40 cm H(2)O and then in steps deflated. MEASUREMENTS AND RESULTS: EIT measurements were performed. Impedance was highly linear with lung volume ( r(2)=0.97). From the pressure-volume maneuver regional pressure-impedance (P-I) curves were obtained in the upper half (ventral) and lower half (dorsal) of the thoracic cross-section. Excellent fit was found of the regional P-I curves with a predefined sigmoid equation ( r(2)=0.998). The P-I curves after lavage were markedly different than before lavage. The P-I curves recorded after lavage displayed a strong heterogeneity on the inflation limb: Lower corner pressure (traditionally lower inflection point) was significantly higher in the dorsal (28.3+/-4.1 cm H(2)O) than in the ventral region (17.5+/-4.3 cm H(2)O). The deflation limb displayed a more homogeneous pattern. Upper corner pressure and true inflection point, where the curve slope is maximal, in the dorsal region were only slightly higher than in the ventral region (1-2 cm H(2)O). CONCLUSIONS: EIT and automated curve fitting provide information on regional lung inflation and deflation which may be of clinical use for optimizing ventilator settings.

Oxygenation index, an indicator of optimal distending pressure during high-frequency oscillatory ventilation?

OBJECTIVE: To test the hypothesis that, during high-frequency oscillatory ventilation (HFOV) of pigs with acute lung injury, the oxygenation index (OI = Paw*FIO(2)*100/PaO(2)) is minimal at the lowest continuous distending pressure (Paw), where the physiological shunt fraction is below 0.1 (Paw(optimal)). DESIGN AND SETTING: Prospective, observational study in a university research laboratory. SUBJECTS: Eight Yorkshire pigs weighing 12.0+/-0.5 kg, with lung injury induced by lung lavage. INTERVENTIONS: After initiation of HFOV, the pigs were subjected to a stepwise increase of Paw to obtain under-inflation, optimal inflation and over-distension of the lungs (inflation) in series, followed by a similar decrease of Paw (deflation). MEASUREMENTS AND RESULTS: At each Paw level, the OI and physiological shunt fraction were determined. The OI reached a minimum of 6.2+/-1.4 at Paw 30+/-4 cmH(2)O during inflation and a minimum of 2.4+/-0.3 at Paw 13+/-2 cmH(2)O during deflation. Paw(optimal) was 32+/-6 cmH(2)O on the inflation limb and 14+/-2 cmH(2)O on the deflation limb. The difference between the Paw at minimal OI and Paw(optimal) was -1.9+/-4.2 cmH(2)O (NS) during inflation and -1.5+/-1.6 cmH(2)O (p<0.05) during deflation. In 15 out of the 16 comparisons, the difference in Paw was within one step (+/-3 cmH(2)O). CONCLUSION: The minimal OI is indicative for the Paw where oxygenation is optimal during HFOV in surfactant-depleted pigs.