Jos R. C. Jansen

An evaluation of cardiac output by five arterial pulse contour techniques during cardiac surgery.

The bias, precision and tracking ability of five different pulse contour methods were evaluated by simultaneous comparison of cardiac output values from the conventional thermodilution technique (COtd). The five different pulse contour methods included in this study were: Wesselings method (cZ); the Modelflow method; the LiDCO system; the PiCCO system and a recently developed Hemac method. We studied 24 cardiac surgery patients undergoing uncomplicated coronary artery bypass grafting. In each patient, the first series of COtd was used to calibrate the five pulse contour methods. In all, 199 series of measurements were accepted by all methods and included in the study. COtd ranged from 2.14 to 7.55 l.min−1, with a mean of 4.81 l.min−1. Bland‐Altman analysis showed the following bias and limits of agreement: cZ, 0.23 and − 0.80 to 1.26 l.min−1; Modelflow, 0.00 and − 0.74 to 0.74 l.min−1; LiDCO, – 0.17 and − 1.55 to 1.20 l.min−1; PiCCO, 0.14 and − 1.60 to 1.89 l.min−1; and Hemac, 0.06 and − 0.81 to 0.93 l.min−1. Changes in cardiac output larger than 0.5 l.min−1 (10%) were correctly followed by the Modelflow and the Hemac method in 96% of cases. In this group of subjects, without congestive heart failure, with normal heart rhythm and reasonable peripheral circulation, the best results in absolute values as well as in tracking changes in cardiac output were measured using the Modelflow and Hemac pulse contour methods, based on non‐linear three‐element Windkessel models.

Beat-to-Beat Analysis of Left Ventricular Pressure-Volume Relation and Stroke Volume by Conductance Catheter and Aortic Modelflow in Cardiomyoplasty Patients

BACKGROUND Since the clinical introduction of dynamic cardiomyoplasty, a discrepancy has been observed between unchanged measurements of cardiac function and improved clinical outcome. METHODS AND RESULTS We performed a beat-to-beat analysis of cardiac performance at rest in nine cardiomyoplasty patients 6 to 24 months after operation. Conductance and micromanometer catheters were placed in left ventricle and aorta and used for measurements over a 15-second period, during which the wrapped latissimus dorsi (LD) muscle was stimulated for 10 seconds in a 1:2 synchronization mode followed by a 5-second period without LD stimulation. The synchronization delay between start of the QRS complex and the LD contraction was changed from 4 up to 125 ms at the patients clinical stimulation strength and at an increased supramaximal amplitude. Comparing the LD assisted period to the unassisted period, at the clinical settings no significant changes in stroke volume (SV) as measured by the conductance technique and the aortic Modelflow technique were observed. A significant (P < .05) rise in left ventricular end-diastolic pressure (LVEDP) was observed directly after the assisted 10-second period. The peak ejection rate (PER) of left ventricular volume increased (P < .05), with a mean of 28 +/- 23% during the LD stimulated beats. At the patients individual best setting, SV of the stimulated beats increased (P < .01) by a mean of 20 +/- 15%. Systolic aortic pressure increased (P < .01) by a mean of 7 mm Hg, peak negative dP/dt increased (P < .01), and PER increased, with a mean of 68 +/- 24% (P < .01). LVEDP was similar in stimulated and unstimulated beats and increased (P < .05) in the nonpaced 5-second period. The delay for the best setting ranged from 25 to 125 ms; the stimulus strength was 1.5 to 3 V higher than the clinical setting. At the patients individual worst setting, SV remained unchanged and PER was higher, with a mean of 30 +/- 25% (P < .05). The worst setting was observed at the 1.5- to 3-V-higher stimulus strength; in six patients, it was at a short delay (4 to 25 ms) and in three patients, at the longest delay (100 to 125 ms). CONCLUSIONS By the left ventricular conductance catheter and aortic Modelflow methods, improvement in cardiac function by dynamic cardiomyoplasty was demonstrated in this patient group. The synchronization interval, stimulus strength, and stimulus duration appeared to be critical for obtaining optimal improvement.

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·mm Hg−1·kg−1 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.

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.

Left Ventricular Pressure-Volume Relationships Before and After Cardiomyoplasty in Patients With Heart Failure

BACKGROUND The aim of this study was to elucidate whether beneficial effects of cardiomyoplasty (CMP) in patients with dilated cardiomyopathy are the result of a decrease in existing ventricular dilatation or a prevention of further dilatation. METHODS AND RESULTS Combined micromanometer-conductance catheters were used to evaluate left ventricular pressure-volume relationships in six patients with dilated cardiomyopathy before and at 6 and 12 months after CMP. Acute changes in preload and afterload were induced by a standardized leg-tilting intervention and a bolus infusion of nitroglycerin. After CMP, end-diastolic volume (EDV) decreased from 138+/-10 to 103+/-18 mL/m2 (P<.01) at 6 months and to 83+/-17 mL/m2 (P<.01) at 12 months. End-diastolic pressure (EDP) decreased from 20.2+/-6.4 to 13.9+/-7.7 mm Hg (P<.01) at 6 months after CMP. Peak ejection rate and ejection fraction increased at 6 months after CMP from 594+/-214 to 799+/-214 mL/s (P<.05) and from 26.6+/-4.7% to 40.1+/-8.3% (P<.05), respectively. Peak dP/dt decreased at 12 months after CMP from -842+/-142 to -712+/-168 mm Hg/s (P<.05). Leg-tilting before CMP increased EDP from 20.2+/-6.4 to 25.6+/-5.2 mm Hg (P<.01), end-systolic pressure (ESP) from 118+/-17 to 122+/-17 mm Hg (P<.05), and tau from 50.8+/-2.8 to 53.8+/-2.3 ms (P<.05). Six months after CMP, leg-tilting also increased EDV from 103+/-18 to 110+/-22 mL/m2 (P<.05) and ESV from 62+/-14 to 66+/-14 mL/m2 (P<.05). Before CMP, nitroglycerin decreased EDP from 20.2+/-6.4 to 10.4+/-3.8 mm Hg (P<.01), ESP from 118+/-17 to 96+/-11 mm Hg (P<.05), ESV from 100+/-11 to 89+/-7 mL/m2 (P<.05), and tau from 50.8+/-2.8 to 44.5+/-3.7 ms (P<.05). Six months after CMP, nitroglycerin decreased EDP, ESP, and tau to similar values. CONCLUSIONS Our findings show that up to 1 year after CMP, marked decreases in left ventricular volume are present. Our measurements suggest that CMP actively reduced the dilated ventricle but did not prevent a higher EDV on an increased venous return. The latissimus dorsi muscle wrap contraction results in better synchronization of contraction and more rapid emptying of the left ventricle.

Performance of three minimally invasive cardiac output monitoring systems

We evaluated cardiac output (CO) using three new methods – the auto‐calibrated FloTrac–Vigileo (COed), the non‐calibrated Modelflow (COmf ) pulse contour method and the ultra‐sound HemoSonic system (COhs) – with thermodilution (COtd) as the reference. In 13 postoperative cardiac surgical patients, 104 paired CO values were assessed before, during and after four interventions: (i) an increase of tidal volume by 50%; (ii) a 10 cm H2O increase in positive end‐expiratory pressure; (iii) passive leg raising and (iv) head up position. With the pooled data the difference (bias (2SD)) between COed and COtd, COmf and COtd and COhs and COtd was 0.33 (0.90), 0.30 (0.69) and −0.41 (1.11) l.min−1, respectively. Thus, Modelflow had the lowest mean squared error, suggesting that it had the best performance. COed significantly overestimates changes in cardiac output while COmf and COhs values are not significantly different from those of COtd. Directional changes in cardiac output by thermodilution were detected with a high score by all three methods.

Peripheral vascular decoupling in porcine endotoxic shock

Cardiac output measurement from arterial pressure waveforms presumes a defined relationship between the arterial pulse pressure (PP), vascular compliance (C), and resistance (R). Cardiac output estimates degrade if these assumptions are incorrect. We hypothesized that sepsis would differentially alter central and peripheral vasomotor tone, decoupling the usual pressure wave propagation from central to peripheral sites. We assessed arterial input impedance (Z), C, and R from central and peripheral arterial pressures, and aortic blood flow in an anesthetized porcine model (n = 19) of fluid resuscitated endotoxic shock induced by endotoxin infusion (7 μg·kg⁻¹·h⁻¹ increased to 14 and 20 μg·kg⁻¹·h⁻¹ every 10 min and stopped when mean arterial pressure <40 mmHg or Sv(O₂) < 45%). Aortic, femoral, and radial artery pressures and aortic and radial artery flows were measured. Z was calculated by FFT of flow and pressure data. R and C were derived using a two-element Windkessel model. Arterial PP increased from aortic to femoral and radial sites. During stable endotoxemia with fluid resuscitation, aortic and radial blood flows returned to or exceeded baseline while mean arterial pressure remained similarly decreased at all three sites. However, aortic PP exceeded both femoral and radial arterial PP. Although Z, R, and C derived from aortic and radial pressure and aortic flow were similar during baseline, Z increases and C decreases when derived from aortic pressure whereas Z decreases and C increases when derived from radial pressure, while R decreased similarly with both pressure signals. This central-to-peripheral vascular tone decoupling, as quantified by the difference in calculated Z and C from aortic and radial artery pressure, may explain the decreasing precision of peripheral arterial pressure profile algorithms in assessing cardiac output in septic shock patients and suggests that different algorithms taking this vascular decoupling into account may be necessary to improve their precision in this patient population.

Single injection thermodilution : A flow-corrected method

Background Application of the Stewart-Hamilton equation in the thermodilution technique requires flow to be constant. In patients in whom ventilation of the lungs is controlled, flow modulations may occur leading to large errors in the estimation of mean cardiac output. Methods To eliminate these errors, a modified equation was developed. The resulting flow-corrected equation needs an additional measure of the relative changes of blood flow during the period of the dilution curve. Relative flow was computed from the pulmonary artery pressure with use of the pulse contour method. Measurements were obtained in 16 patients undergoing elective coronary artery bypass surgery. In 11 patients (group A), pulmonary artery pressure was measured with a catheter tip transducer, in a partially overlapping group of 11 patients (group B), it was measured with a fluid-filled system. For reference cardiac output we used the proven method of four uncorrected thermodilution estimates equally spread over the ventilatory cycle. Results A total of 208 cardiac output estimates was obtained in group A, and 228 in group B. In group B, 48 estimates could not be corrected because of insufficient pulmonary artery pressure waveform quality from the fluid-filled system. Individual uncorrected Stewart-Hamilton estimates showed a large variability with respect to their mean. In group A, mean cardiac output was 5.01 l/min with a standard deviation of 0.53 l/min, or 10.6%. After flow correction, this scatter decreased to 5.0% (P < 0.0001). With no bias, the corresponding limits of agreement decreased from plus/minus 1.06 to plus/minus 0.5 l/min after flow correction. In group B, the scatter decreased similarly and the limits of agreement also became plus/minus 0.5 l/min after flow correction. Conclusion It was concluded that a single thermodilution cardiac output estimate using the flow-corrected equation is clinically feasible. This is obtained at the cost of a more complex computation and an extra pressure measurement, which often is already available. With this technique it is possible to reduce the fluid load to the patient considerably.

Bedside assessment of mean systemic filling pressure.

Purpose of reviewThe 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 findingsUsing 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. SummaryMeasurement 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.

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.