The Experts below are selected from a list of 17703 Experts worldwide ranked by ideXlab platform
Michael R Pinsky - One of the best experts on this subject based on the ideXlab platform.
-
cardiac output response to norepinephrine in postoperative cardiac surgery patients interpretation with Venous Return and cardiac function curves
Critical Care Medicine, 2013Co-Authors: Jacinta J Maas, Michael R Pinsky, Rob P De Wilde, Eve De Jonge, Jos R C JanseAbstract: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)
-
Effect of positive pressure on Venous Return in volume-loaded cardiac surgical patients.
Journal of Applied Physiology, 2002Co-Authors: Paul C. M. Van Den Berg, Jos R. C. Jansen, Michael R PinskyAbstract:The hemodynamic effects of increases in airway pressure (Paw) are related in part to Paw-induced increases in right atrial pressure (Pra), the downstream pressure for Venous Return, thus decreasing...
-
effect of positive pressure on Venous Return in volume loaded cardiac surgical patients
Journal of Applied Physiology, 2002Co-Authors: Paul C M Van Den Berg, Jos R. C. Jansen, Michael R PinskyAbstract:The hemodynamic effects of increases in airway pressure (Paw) are related in part to Paw-induced increases in right atrial pressure (Pra), the downstream pressure for Venous Return, thus decreasing the pressure gradient for Venous Return. However, numerous animal and clinical studies have shown that Venous Return is often sustained during ventilation with positive end-expiratory pressure (PEEP). Potentially, PEEP-induced diaphragmatic descent increases abdominal pressure (Pabd). We hypothesized that an increase in Paw induced by PEEP would minimally alter Venous Return because the associated increase in Pra would be partially offset by a concomitant increase in Pabd. Thus we studied the acute effects of graded increases of Paw on Pra, Pabd, and cardiac output by application of inspiratory-hold maneuvers in sedated and paralyzed humans. Forty-two patients were studied in the intensive care unit after coronary artery bypass surgery during hemodynamically stable, fluid-resuscitated conditions. Paw was progressively increased in steps of 2 to 4 cmH(2)O from 0 to 20 cmH(2)O in sequential 25-s inspiratory-hold maneuvers. Right ventricular (RV) cardiac output (CO(td)) and RV ejection fraction (EF(rv)) were measured at 5 s into the inspiratory-hold maneuver by the thermodilution technique. RV end-diastolic volume and stroke volume were calculated from EF(rv) and heart rate data, and Pra was measured from the pulmonary artery catheter. Pabd was estimated as bladder pressure. We found that, although increasing Paw progressively increased Pra, neither CO(td) nor RV end-diastolic volume changed. The ratio of change (Delta) in Paw to Delta Pra was 0.32 +/- 0.20. The ratio of Delta Pra to Delta CO(td) was 0.05 +/- 00.15 l x min(-1) x mmHg(-1). However, Pabd increased such that the ratio of Delta Pra to Delta Pabd was 0.73 +/- 0.36, meaning that most of the increase in Pra was reflected in increases in Pabd. We conclude that, in hemodynamically stable fluid-resuscitated postoperative surgical patients, inspiratory-hold maneuvers with increases in Paw of up to 20 cmH(2)O have minimal effects on cardiac output, primarily because of an in-phase-associated pressurization of the abdominal compartment associated with compression of the liver and squeezing of the lungs.
G L Brengelmann - One of the best experts on this subject based on the ideXlab platform.
-
Venous Return and the physical connection between distribution of segmental pressures and volumes
American Journal of Physiology-heart and Circulatory Physiology, 2019Co-Authors: G L BrengelmannAbstract:More than sixty years ago, Guyton and coworkers related their observations of Venous Return to a mathematical model. Showing steady-state flow (F) as proportional to the difference between mean sys...
-
Venous Return mean systemic pressure and getting the right answer for the wrong reason
Annals of Translational Medicine, 2019Co-Authors: G L BrengelmannAbstract:Berger and Takala, in their recent article in this journal (1), adhere to the view that Venous Return (VR), determines cardiac output (CO) because the heart can only pump out what it receives1. They see VR as driven by mean systemic pressure (Pms), which is opposed by the pressure at the right atrium (Pra).
-
letter to the editor why persist in the fallacy that mean systemic pressure drives Venous Return
American Journal of Physiology-heart and Circulatory Physiology, 2016Co-Authors: G L BrengelmannAbstract:to the editor: The work of Berger et al. ([3][1]), recently published in the American Journal of Physiology-Heart and Circulatory Physiology , has at its core the idea that steady-state Venous Return (F) is driven through the resistance to Venous Return (Rven) by the difference between mean systemic
-
a critical analysis of the view that right atrial pressure determines Venous Return
Journal of Applied Physiology, 2003Co-Authors: G L BrengelmannAbstract:A. C. Guyton pioneered major advances in understanding cardiovascular equilibrium. He superimposed Venous Return curves on cardiac output curves to reveal their intersection at the one level of rig...
Jukka Takala - One of the best experts on this subject based on the ideXlab platform.
-
determinants of systemic Venous Return and the impact of positive pressure ventilation
Annals of Translational Medicine, 2018Co-Authors: David H Berger, Jukka TakalaAbstract:Venous Return, i.e., the blood flowing back to the heart, is driven by the pressure difference between mean systemic filling pressure and right atrial pressure (RAP). Besides cardiac function, it is the major determinant of cardiac output. Mean systemic filling pressure is a function of the vascular volume. The concept of Venous Return has a central role for heart lung interactions and the explanation of shock states. Mechanical ventilation during anaesthesia and critical illness may severely affect Venous Return by different mechanisms. In the first part of the following article, we will discuss the development of the concept of Venous Return, its specific components mean systemic and mean circulatory filling pressure (MCFP), RAP and resistance to Venous Return (RVR). We show how these pressures relate to the volume state of the circulation. Various interpretations and critiques are elucidated. In the second part, we focus on the impact of positive pressure ventilation on Venous Return and its components, including latest results from latest research.
-
right atrial pressure and Venous Return during cardiopulmonary bypass
American Journal of Physiology-heart and Circulatory Physiology, 2017Co-Authors: Jukka Takala, Per Werner Moller, Berhard Winkler, Samuel Hurni, Paul Philipp Heinisch, Andreas Bloch, Soren Sondergaard, Stephan M Jakob, David H BergerAbstract:The relevance of right atrial pressure (RAP) as the backpressure for Venous Return (QVR) and mean systemic filling pressure as upstream pressure is controversial during dynamic changes of circulation. To examine the immediate response of QVR (sum of caval vein flows) to changes in RAP and pump function, we used a closed-chest, central cannulation, heart bypass porcine preparation (n = 10) with venoarterial extracorporeal membrane oxygenation. Mean systemic filling pressure was determined by clamping extracorporeal membrane oxygenation tubing with open or closed arterioVenous shunt at euvolemia, volume expansion (9.75 ml/kg hydroxyethyl starch), and hypovolemia (bleeding 19.5 ml/kg after volume expansion). The responses of RAP and QVR were studied using variable pump speed at constant airway pressure (PAW) and constant pump speed at variable PAW Within each volume state, the immediate changes in QVR and RAP could be described with a single linear regression, regardless of whether RAP was altered by pump speed or PAW (r2 = 0.586-0.984). RAP was inversely proportional to pump speed from zero to maximum flow (r2 = 0.859-0.999). Changing PAW caused immediate, transient, directionally opposite changes in RAP and QVR (RAP: P ≤ 0.002 and QVR: P ≤ 0.001), where the initial response was proportional to the change in QVR driving pressure. Changes in PAW generated volume shifts into and out of the right atrium, but their effect on upstream pressure was negligible. Our findings support the concept that RAP acts as backpressure to QVR and that Guyton's model of circulatory equilibrium qualitatively predicts the dynamic response from changing RAP.NEW & NOTEWORTHY Venous Return responds immediately to changes in right atrial pressure. Concomitant volume shifts within the systemic circulation due to an imbalance between cardiac output and Venous Return have negligible effects on mean systemic filling pressure. Guyton's model of circulatory equilibrium can qualitatively predict the resulting changes in dynamic conditions with right atrial pressure as backpressure to Venous Return.
-
reply to letter to the editor why persist in the fallacy that mean systemic pressure drives Venous Return
American Journal of Physiology-heart and Circulatory Physiology, 2016Co-Authors: David H Berger, Per Werner Moller, Jukka TakalaAbstract:reply: We thank Dr. Brengelmann for his comments ([2][1]) to our recent article ([1][2]) appearing in the American Journal of Physiology-Heart and Circulatory Physiology . Brengelmann highlights the controversies on Guyton's concepts of Venous Return. He raises 10 important issues. First, how
-
effect of peep blood volume and inspiratory hold maneuvers on Venous Return
American Journal of Physiology-heart and Circulatory Physiology, 2016Co-Authors: David H Berger, Per Werner Moller, Andreas Bloch, Soren Sondergaard, Stephan M Jakob, Alberto Weber, Stefan Bloechlinger, Matthias Haenggi, Sheldon Magder, Jukka TakalaAbstract:According to Guyton's model of circulation, mean systemic filling pressure (MSFP), right atrial pressure (RAP), and resistance to Venous Return (RVR) determine Venous Return. MSFP has been estimated from inspiratory hold-induced changes in RAP and blood flow. We studied the effect of positive end-expiratory pressure (PEEP) and blood volume on Venous Return and MSFP in pigs. MSFP was measured by balloon occlusion of the right atrium (MSFPRAO), and the MSFP obtained via extrapolation of pressure-flow relationships with airway occlusion (MSFPinsp_hold) was extrapolated from RAP/pulmonary artery flow (QPA) relationships during inspiratory holds at PEEP 5 and 10 cmH2O, after bleeding, and in hypervolemia. MSFPRAO increased with PEEP [PEEP 5, 12.9 (SD 2.5) mmHg; PEEP 10, 14.0 (SD 2.6) mmHg, P = 0.002] without change in QPA [2.75 (SD 0.43) vs. 2.56 (SD 0.45) l/min, P = 0.094]. MSFPRAO decreased after bleeding and increased in hypervolemia [10.8 (SD 2.2) and 16.4 (SD 3.0) mmHg, respectively, P < 0.001], with parallel changes in QPA Neither PEEP nor volume state altered RVR (P = 0.489). MSFPinsp_hold overestimated MSFPRAO [16.5 (SD 5.8) vs. 13.6 (SD 3.2) mmHg, P = 0.001; mean difference 3.0 (SD 5.1) mmHg]. Inspiratory holds shifted the RAP/QPA relationship rightward in euvolemia because inferior vena cava flow (QIVC) recovered early after an inspiratory hold nadir. The QIVC nadir was lowest after bleeding [36% (SD 24%) of preinspiratory hold at 15 cmH2O inspiratory pressure], and the QIVC recovery was most complete at the lowest inspiratory pressures independent of volume state [range from 80% (SD 7%) after bleeding to 103% (SD 8%) at PEEP 10 cmH2O of QIVC before inspiratory hold]. The QIVC recovery thus defends Venous Return, possibly via hepatosplanchnic vascular waterfall.
Jerome A Dempsey - One of the best experts on this subject based on the ideXlab platform.
-
Skeletal muscle pump versus respiratory muscle pump: modulation of Venous Return from the locomotor limb in humans
The Journal of Physiology, 2005Co-Authors: Jordan D. Miller, David F Pegelow, Anthony J Jacques, Jerome A DempseyAbstract:The vast majority of quantitative data examining the effects of breathing on Venous Return have been derived from anaesthetized or reduced animal preparations, making an extrapolation to an upright exercising human problematic due to the lack of a hydrostatic column and an absence of muscular contraction. Thus, this study is the first to quantitatively examine the effects of different breathing mechanics on Venous Return from the locomotor limbs both at rest and during calf contraction exercise in the semirecumbent human. When subjects inspired using predominantly their ribcage/accessory inspiratory muscles at rest (change in gastric pressure (ΔPGA) = 5 cmH2O, ΔPES=∼−6 cmH2O; TI/TTOT= 0.5), femoral Venous Return was markedly impeded (net retrograde flow of 11%) and significantly lower than that observed during ribcage breathing conditions (P < 0.01). During the ensuing expiratory phase of a diaphragmatic breath, there was a large resurgence of femoral Venous blood flow. The pattern of modulation during ribcage and diaphragmatic breathing persisted during both mild (peak calf force = 7 kg) and moderate (peak calf force = 11 kg) levels of calf contraction. Despite the significant within-breath modulation of femoral Venous Return by breathing, net blood flow in the steady state was not altered by the breathing pattern followed by the subjects. Though popliteal blood flow appeared to be modulated by respiration at rest, this pattern was absent during mild calf contraction where popliteal outflow was phasic with the concentric phase of calf contraction. We conclude that respiratory muscle pressure production is the predominant factor modulating Venous Return from the locomotor limb both at rest and during calf contraction even when the veins of the lower limb are distended due to the presence of a physiologic hydrostatic column.
-
Skeletal muscle pump versus respiratory muscle pump: modulation of Venous Return from the locomotor limb in humans.
The Journal of physiology, 2005Co-Authors: Jordan D. Miller, David F Pegelow, Anthony J Jacques, Jerome A DempseyAbstract:The vast majority of quantitative data examining the effects of breathing on Venous Return have been derived from anaesthetized or reduced animal preparations, making an extrapolation to an upright exercising human problematic due to the lack of a hydrostatic column and an absence of muscular contraction. Thus, this study is the first to quantitatively examine the effects of different breathing mechanics on Venous Return from the locomotor limbs both at rest and during calf contraction exercise in the semirecumbent human. When subjects inspired using predominantly their ribcage/accessory inspiratory muscles at rest (change in gastric pressure (DeltaP(GA)) = 5 cmH(2)O, DeltaP(ES) = approximately -6 cmH(2)O; T(I)/T(TOT) = 0.5), femoral Venous Return was markedly impeded (net retrograde flow of 11%) and significantly lower than that observed during ribcage breathing conditions (P < 0.01). During the ensuing expiratory phase of a diaphragmatic breath, there was a large resurgence of femoral Venous blood flow. The pattern of modulation during ribcage and diaphragmatic breathing persisted during both mild (peak calf force = 7 kg) and moderate (peak calf force = 11 kg) levels of calf contraction. Despite the significant within-breath modulation of femoral Venous Return by breathing, net blood flow in the steady state was not altered by the breathing pattern followed by the subjects. Though popliteal blood flow appeared to be modulated by respiration at rest, this pattern was absent during mild calf contraction where popliteal outflow was phasic with the concentric phase of calf contraction. We conclude that respiratory muscle pressure production is the predominant factor modulating Venous Return from the locomotor limb both at rest and during calf contraction even when the veins of the lower limb are distended due to the presence of a physiologic hydrostatic column.
Per Werner Moller - One of the best experts on this subject based on the ideXlab platform.
-
right atrial pressure and Venous Return during cardiopulmonary bypass
American Journal of Physiology-heart and Circulatory Physiology, 2017Co-Authors: Jukka Takala, Per Werner Moller, Berhard Winkler, Samuel Hurni, Paul Philipp Heinisch, Andreas Bloch, Soren Sondergaard, Stephan M Jakob, David H BergerAbstract:The relevance of right atrial pressure (RAP) as the backpressure for Venous Return (QVR) and mean systemic filling pressure as upstream pressure is controversial during dynamic changes of circulation. To examine the immediate response of QVR (sum of caval vein flows) to changes in RAP and pump function, we used a closed-chest, central cannulation, heart bypass porcine preparation (n = 10) with venoarterial extracorporeal membrane oxygenation. Mean systemic filling pressure was determined by clamping extracorporeal membrane oxygenation tubing with open or closed arterioVenous shunt at euvolemia, volume expansion (9.75 ml/kg hydroxyethyl starch), and hypovolemia (bleeding 19.5 ml/kg after volume expansion). The responses of RAP and QVR were studied using variable pump speed at constant airway pressure (PAW) and constant pump speed at variable PAW Within each volume state, the immediate changes in QVR and RAP could be described with a single linear regression, regardless of whether RAP was altered by pump speed or PAW (r2 = 0.586-0.984). RAP was inversely proportional to pump speed from zero to maximum flow (r2 = 0.859-0.999). Changing PAW caused immediate, transient, directionally opposite changes in RAP and QVR (RAP: P ≤ 0.002 and QVR: P ≤ 0.001), where the initial response was proportional to the change in QVR driving pressure. Changes in PAW generated volume shifts into and out of the right atrium, but their effect on upstream pressure was negligible. Our findings support the concept that RAP acts as backpressure to QVR and that Guyton's model of circulatory equilibrium qualitatively predicts the dynamic response from changing RAP.NEW & NOTEWORTHY Venous Return responds immediately to changes in right atrial pressure. Concomitant volume shifts within the systemic circulation due to an imbalance between cardiac output and Venous Return have negligible effects on mean systemic filling pressure. Guyton's model of circulatory equilibrium can qualitatively predict the resulting changes in dynamic conditions with right atrial pressure as backpressure to Venous Return.
-
reply to letter to the editor why persist in the fallacy that mean systemic pressure drives Venous Return
American Journal of Physiology-heart and Circulatory Physiology, 2016Co-Authors: David H Berger, Per Werner Moller, Jukka TakalaAbstract:reply: We thank Dr. Brengelmann for his comments ([2][1]) to our recent article ([1][2]) appearing in the American Journal of Physiology-Heart and Circulatory Physiology . Brengelmann highlights the controversies on Guyton's concepts of Venous Return. He raises 10 important issues. First, how
-
effect of peep blood volume and inspiratory hold maneuvers on Venous Return
American Journal of Physiology-heart and Circulatory Physiology, 2016Co-Authors: David H Berger, Per Werner Moller, Andreas Bloch, Soren Sondergaard, Stephan M Jakob, Alberto Weber, Stefan Bloechlinger, Matthias Haenggi, Sheldon Magder, Jukka TakalaAbstract:According to Guyton's model of circulation, mean systemic filling pressure (MSFP), right atrial pressure (RAP), and resistance to Venous Return (RVR) determine Venous Return. MSFP has been estimated from inspiratory hold-induced changes in RAP and blood flow. We studied the effect of positive end-expiratory pressure (PEEP) and blood volume on Venous Return and MSFP in pigs. MSFP was measured by balloon occlusion of the right atrium (MSFPRAO), and the MSFP obtained via extrapolation of pressure-flow relationships with airway occlusion (MSFPinsp_hold) was extrapolated from RAP/pulmonary artery flow (QPA) relationships during inspiratory holds at PEEP 5 and 10 cmH2O, after bleeding, and in hypervolemia. MSFPRAO increased with PEEP [PEEP 5, 12.9 (SD 2.5) mmHg; PEEP 10, 14.0 (SD 2.6) mmHg, P = 0.002] without change in QPA [2.75 (SD 0.43) vs. 2.56 (SD 0.45) l/min, P = 0.094]. MSFPRAO decreased after bleeding and increased in hypervolemia [10.8 (SD 2.2) and 16.4 (SD 3.0) mmHg, respectively, P < 0.001], with parallel changes in QPA Neither PEEP nor volume state altered RVR (P = 0.489). MSFPinsp_hold overestimated MSFPRAO [16.5 (SD 5.8) vs. 13.6 (SD 3.2) mmHg, P = 0.001; mean difference 3.0 (SD 5.1) mmHg]. Inspiratory holds shifted the RAP/QPA relationship rightward in euvolemia because inferior vena cava flow (QIVC) recovered early after an inspiratory hold nadir. The QIVC nadir was lowest after bleeding [36% (SD 24%) of preinspiratory hold at 15 cmH2O inspiratory pressure], and the QIVC recovery was most complete at the lowest inspiratory pressures independent of volume state [range from 80% (SD 7%) after bleeding to 103% (SD 8%) at PEEP 10 cmH2O of QIVC before inspiratory hold]. The QIVC recovery thus defends Venous Return, possibly via hepatosplanchnic vascular waterfall.
