Jacinta J. Maas

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.

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.

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.

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.

A mini-fluid challenge of 150 mL predicts fluid responsiveness using Modelflow R 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.