Rob B. P. de Wilde

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 &mgr;g·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.

Pulse Contour Analysis to Assess Hemodynamic Response to Passive Leg Raising

OBJECTIVE The authors evaluated the ability of 2 pulse contour cardiac output (CO) techniques to track CO changes during passive leg raising (PLR) to assess fluid loading responsiveness. DESIGN A prospective study. SETTING An intensive care unit in a university hospital. PARTICIPANTS Twenty mechanically ventilated postoperative cardiac surgery patients. INTERVENTIONS Thirty-degree PLR. MEASUREMENTS AND MAIN RESULTS The authors estimated CO by 3 techniques: thermodilution (COtd), arterial pulse power (Coli; LiDCO, London, UK), and pulse contour method (Com; FMS, Amsterdam, The Netherlands) based on uncalibrated Modelflow. The authors measured heart rate (HR), central venous pressure, arterial pulse pressure (PP), systolic pressure (SP), and mean arterial pressure (MAP). Stroke volume (SV), SP, PP, and SV variation (PPV and SVV, respectively) were calculated over 5 breaths. SVV was measured by both LiDCO (SVVli) and Modelflow (SVVm) devices. PLR-induced changes in COtd correlated with COli (p < 0.001) and COm (p < 0.001). Preload dependence was predicted with an area under the ROC curve of 0.968 for ΔCOm, 0.841 for ΔCOli, 0.825 for SVVm, 0.873 for SVVli, 0.808 for PPV, 0.778 for ΔSP, 0.714 for ΔPP, and 0.873 for ΔMAP. CONCLUSIONS Changes in COm, COli, SVV, and PPV track COtd changes during PLR with a high degree of accuracy in sedated, ventilated, postoperative cardiac surgery patients. Changes in pulse contour CO after PLR can be used to predict fluid loading responsiveness.

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.

Relative value of pressures and volumes in assessing fluid responsiveness after valvular and coronary artery surgery

BACKGROUND AND AIMS Cardiac function may differ after valvular (VS) and coronary artery (CAS) surgery and this may affect assessment of fluid responsiveness. The aim of the study was to compare VS and CAS in the value of cardiac filling pressures and volumes herein. METHODS There were eight consecutive patients after VS and eight after CAS, with femoral and pulmonary artery catheters in place. In each patient, five sequential fluid loading steps of 250 ml of colloid each were done. We measured central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP) and, by transpulmonary thermodilution, cardiac index (CI) and global end-diastolic (GEDVI) and intrathoracic blood volume (ITBVI) indices. Fluid responsiveness was defined by a CI increase >5% or >10% per step. RESULTS Global ejection fraction was lower and PAOP was higher after VS than CAS. In responding steps after VS (n=9-14) PAOP and volumes increased, while CVP and volumes increased in responding steps (n=12-19) after CAS. Baseline PAOP was lower in responding steps after VS only. Hence, baseline PAOP as well as changes in PAOP and volumes were of predictive value after VS and changes in CVP and volumes after CAS, in receiver operating characteristic curves. After VS, PAOP and volume changes equally correlated to CI changes. After CAS, only changes in CVP and volumes correlated to those in CI. CONCLUSIONS While volumes are equally useful in monitoring fluid responsiveness, the predictive and monitoring value of PAOP is greater after VS than after CAS. In contrast, the CVP is of similar value as volume measurements in monitoring fluid responsiveness after CAS. The different value of pressures rather than of volumes between surgery types is likely caused by systolic left ventricular dysfunction in VS. The study suggests an effect of systolic cardiac function on optimal parameters of fluid responsiveness and superiority of the pulmonary artery catheter over transpulmonary dilution, for haemodynamic monitoring of VS patients.

PReVENT - protective ventilation in patients without ARDS at start of ventilation: study protocol for a randomized controlled trial

BackgroundIt is uncertain whether lung-protective mechanical ventilation using low tidal volumes should be used in all critically ill patients, irrespective of the presence of the acute respiratory distress syndrome (ARDS). A low tidal volume strategy includes use of higher respiratory rates, which could be associated with increased sedation needs, a higher incidence of delirium, and an increased risk of patient-ventilator asynchrony and ICU-acquired weakness. Another alleged side-effect of low tidal volume ventilation is the risk of atelectasis. All of these could offset the beneficial effects of low tidal volume ventilation as found in patients with ARDS.Methods/DesignPReVENT is a national multicenter randomized controlled trial in invasively ventilated ICU patients without ARDS with an anticipated duration of ventilation of longer than 24 hours in 5 ICUs in The Netherlands. Consecutive patients are randomly assigned to a low tidal volume strategy using tidal volumes from 4 to 6 ml/kg predicted body weight (PBW) or a high tidal volume ventilation strategy using tidal volumes from 8 to 10 ml/kg PBW. The primary endpoint is the number of ventilator-free days and alive at day 28. Secondary endpoints include ICU and hospital length of stay (LOS), ICU and hospital mortality, the incidence of pulmonary complications, including ARDS, pneumonia, atelectasis, and pneumothorax, the cumulative use and duration of sedatives and neuromuscular blocking agents, incidence of ICU delirium, and the need for decreasing of instrumental dead space.DiscussionPReVENT is the first randomized controlled trial comparing a low tidal volume strategy with a high tidal volume strategy, in patients without ARDS at onset of ventilation, that recruits a sufficient number of patients to test the hypothesis that a low tidal volume strategy benefits patients without ARDS with regard to a clinically relevant endpoint.Trial registrationThe trial is registered at www.clinicaltrials.gov under reference number NCT02153294 on 23 May 2014.

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.

Extracorporeal Membrane Oxygenation in Single Ventricle Lesions Palliated Via the Hybrid Approach

Background: Describing outcomes for children with hypoplastic left heart syndrome (HLHS) undergoing hybrid palliation (pulmonary artery band and stent placement in the patent ductus arteriosus) requiring extracorporeal membrane oxygenation (ECMO) support for cardiorespiratory failure. Methods: We reviewed the Extracorporeal Life Support Organization database for all patients with a diagnosis of an HLHS undergoing hybrid stage 1 palliation supported with ECMO and those patients with hybrid palliation supported with ECMO after comprehensive stage 2 palliation. Patients were identified using a combination of International Classification of Diseases, Ninth Revision and registry diagnosis and procedure codes. We report survival to hospital discharge and ECMO complications. Results: We identified 44 patients with HLHS requiring ECMO following stage 1 hybrid approach. Median age at cannulation was 13.5 days. Only 16% survived to hospital discharge. In all, 20 (50%) patients had a cardiac arrest prior to going onto ECMO and for 3 (19%) patients, ECMO was initiated during cardiopulmonary resuscitation. Conclusions: Overall survival for ECMO support in patients with HLHS palliated via the hybrid approach is very poor (16%) and is worse than 31% survival reported for ECMO after conventional stage 1 palliation. The reasons for these poor outcomes require further investigation.

Transpulmonary versus continuous thermodilution cardiac output after valvular and coronary artery surgery

Residual left-sided valvular insufficiencies after valvular surgery may confound transpulmonary thermodilution cardiac output (COtp). We compared the technique with the continuous right-sided thermodilution technique (CCO) after valvular surgery (n=8) and coronary artery surgery (n=8). Patients with pulmonary and femoral artery catheters in the intensive care unit (ICU) were included. After valvular surgery, there was minimal aortic insufficiency in four patients and minimal to moderate mitral valve insufficiency in six. Five fluid loading steps (250 ml) were done in each patient. CCO and COtp were measured prior to and 15 min after each step. The cardiac output was lower after valvular than coronary artery surgery but responses to fluid loading steps were similar among surgery types and techniques. After valvular and coronary artery surgery, cardiac output was lower prior to responses than in non-responses to fluids, by either technique. After valvular surgery, COtp and CCO correlated (r=0.64, P<0.001, n=48) but fluid-induced changes did not. After coronary artery surgery, COtp and CCO correlated (r=0.81, P<0.001) and changes also did (r=0.55, P<0.001). At fluid-induced CCO increases <20%, the r for changes in cardiac output measured by both techniques was similar after valvular and coronary artery surgery. Thus, COtp and CCO were of similar value in predicting and monitoring fluid responses after both surgery types. This argues against left-sided valvular insufficiencies confounding COtp.

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.

Less invasive indicators of changes in thermodilution cardiac output by ventilatory changes after cardiac surgery.

Background and objective We studied whether changes in less invasive, noncalibrated pulse-contour cardiac output (by modified ModelFlow, COmf) and derived stroke volume variations (SVV), as well as systolic and pulse pressure variations, predict changes in bolus thermodilution cardiac output (COtd), evoked by continuous and cyclic increases in intrathoracic pressure by increases in positive end-expiratory pressure (PEEP) and tidal volume (Vt), respectively. Methods Prospective study on 17 critically ill postcardiac surgery patients on full mechanical ventilatory support, in the intensive care unit. Results In contrast to systolic pressure variation and pulse pressure variation, SVV increased from (mean ± SD) 6.2 ± 4.4 to 8.1 ± 5.6 at PEEP 10 cmH2O (P = 0.064) and to 7.8 ± 3.5% at PEEP 15 cmH2O (P = 0.031), concomitantly with a 12 ± 7 and 11 ± 8% decrease in COmf and COtd (P < 0.001), respectively. For pooled data, changes in COmf correlated with those in COtd (r = 0.55, P = 0.002), but changes in SVV did not. Variables did not change when Vt was increased up to 50%. Conclusion A fall in COmf is more sensitive than a rise in SVV, which is more sensitive than systolic pressure variation and pulse pressure variation, in tracking a fall in COtd during continuous (and not cyclic) increases in intrathoracic pressure, in mechanically ventilated patients after cardiac surgery. This suggests a reduction in biventricular preload as the main factor in decreasing cardiac output and increasing SVV with PEEP.