Pressure Gradient For Venous Return Research Articles

Volume responsiveness revisited: an observational multicenter study of continuous versus binary outcomes combining echocardiography and venous return physiology.

Echocardiography can assess cardiac preload when fluid administration is used to treat acute circulatory failure. Changes in stroke volume (SV) are inherently a continuous phenomenon relating to the pressure gradient for venous return (VRdP). However, most clinical studies have applied a binary definition based on a fractional change in SV. This study tested the hypothesis that calculating the analog mean systemic filling pressure (Pmsa) and VRdP would enhance echocardiography to describe SV responses to a preload challenge. We investigated 540 (379 males) patients during a standardized passive leg raising (PLR) maneuver. Patients were further categorized by the presence of impaired right ventricular function (impRV) or increased intra-abdominal hypertension (IAH). Multivariable linear regression identified VRdP (partial r = -0.26, P < 0.001), ventilatory-induced variations in superior vena cava diameter (partial r = 0.43, P < 0.001), and left ventricular outflow tract maximum-Doppler velocity (partial r = 0.13, P < 0.001) as independent variables associated with SV changes. The model explained 38% (P < 0.001) of the SV change in the whole cohort and 64% (P < 0.001) when excluding patients with impRV or IAH. The correlation between Pmsa or VRdP and SV changes lost statistical significance with increasing impRV or IAH. A binary definition of volume responsiveness (>10% increase in SV) generated an area under the curve of 0.79 (P < 0.001) in logistic regression but failed to identify Pmsa or VRdP as independent variables and overlooked the confounding influence of impRV and IAH. In conclusion, venous return physiology may enhance echocardiographic assessments of volume responsiveness, which should be based on continuous changes in stroke volume.NEW & NOTEWORTHY The analog mean systemic filling pressure and the pressure gradient for venous return combined with echocardiography predict continuous changes in stroke volume following a passive leg raising maneuver. The confounding effects of impaired right ventricular function and increased intra-abdominal pressure can be identified. Using a binary cutoff for the fractional change in stroke volume, common in previous clinical research, fails to identify the importance of variables relevant to venous return physiology and confounding conditions.

Changes in mean systemic filling pressure as an estimate of hemodynamic response to anesthesia induction using propofol

BackgroundEven a small change in the pressure gradient between the venous system and the right atrium can have significant hemodynamic effects. Mean systemic filling pressure (MSFP) is the driving force of the venous system. As a result, MSFP has a significant effect on cardiac output. We aimed to test the hypothesis that the hemodynamic instability during induction of general anesthesia by intravenous propofol administration is caused by changes in MSFP.MethodsWe prospectively collected data from 15 patients undergoing major surgery requiring invasive hemodynamic monitoring. Hemodynamic parameters, including MSFP, were measured before and after propofol administration and following intubation, using venous return curves at a no-flow state induced by a pneumatic tourniquet.ResultsA significant decrease in MSFP was observed in all study patients after propofol administration (median (IQR) pressure 17 (9) mmHg compared with 25 (7) before propofol administration, p = 0.001). The pressure gradient for venous return (MSFP – central venous pressure; CVP) also decreased following propofol administration from 19 (8) to 12 (6) mmHg, p = 0.001. Central venous pressure did not change.ConclusionsThese results support the hypothesis that induction of anesthesia with propofol causes a marked reduction in MSFP. A possible mechanism of propofol-induced hypotension is reduction in preload due to a decrease in the venous vasomotor tone.

Effect of norepinephrine challenge on cardiovascular determinants assessed using a mathematical model in septic shock: a physiological study.

The present study investigated the cardiovascular determinants of cardiac output (CO), mean systemic filling pressure analogue (Pmsa) derived by Geoffrey Parkin, efficiency of heart (Eh) and related parameters to a norepinephrine (NE) challenge [an increase of 10 mmHg mean arterial pressure (MAP) by NE] in septic shock patients using of a mathematical model. Twenty-seven septic shock patients with pulse index continuous cardiac output (PiCCO) monitoring were enrolled. These patients required NE to maintain an individualized MAP for organ perfusion after early fluid resuscitation based on their clinical condition. NE was decreased to obtain a decrease of 10 mmHg from base MAP (MAP-10mmHg), and the NE doses were adjusted to return MAP to baseline (MAPbase) and produce an increase of 10 mmHg from MAPbase (MAP+10mmHg). Two NE challenge episodes were analyzed for each patient: from MAP-10mmHg to MAPbase and from MAPbase to MAP+10mmHg. The Pmsa, pressure gradient for venous return (PGvr), and Eh (PGvr relative to Pmsa) were estimated using a mathematical model for the three MAP levels (MAP-10mmHg, MAPbase and MAP+10mmHg). A total of 54 episodes of NE challenges were obtained in 27 patients. Significant and consistent increases were observed in the central venous pressure (CVP), Pmsa, and PGvr in response during the NE titration. ΔCO negatively and significantly correlated with ΔCVP (r=-0.722, P<0.0001), ΔPmsa (r=-0.549, P<0.0001), ΔResistance of venous return (Rvr) (r=-0.597, P<0.0001), and ΔResistance of systemic vascular beds (Rsys) (r=-0.597, P<0.0001). Episodes of decreasing CO/Eh were associated with a higher ΔCVP than the CO/Eh-increasing episodes. The area under the curve (AUC) of ΔCVP to predict decreased CO by the incremental NE was 0.86, and the AUC of ΔCVP to predict decreased Eh was 0.94. A cutoff of ΔCVP >1.5 mmHg for detecting decreased CO resulted in a sensitivity of 75% and a specificity of 94.1%. A cutoff of ΔCVP >1.5 mmHg for detecting decreased Eh resulted in a sensitivity of 64.3% and a specificity of 100%. There were a highly divergent response in Eh and CO to afterload challenge episodes of an NE-induced 10mmHg increase in MAP. An increase in CVP may be an early alarm to identify the reduction in CO/Eh during an NE-induced increase of MAP.

Vasopressor Responsiveness Beyond Arterial Pressure: A Conceptual Systematic Review Using Venous Return Physiology.

We performed a systematic review to investigate the effects of vasopressor-induced hemodynamic changes in adults with shock. We applied a physiological approach using the interacting domains of intravascular volume, heart pump performance, and vascular resistance to structure the interpretation of responses to vasopressors. We hypothesized that incorporating changes in determinants of cardiac output and vascular resistance better reflect the vasopressor responsiveness beyond mean arterial pressure alone.We identified 28 studies including 678 subjects in Pubmed, EMBASE, and CENTRAL databases.All studies demonstrated significant increases in mean arterial pressure (MAP) and systemic vascular resistance during vasopressor infusion. The calculated mean systemic filling pressure analogue increased (16 ± 3.3 mmHg to 18 ± 3.4 mmHg; P = 0.02) by vasopressors with variable effects on central venous pressure and the pump efficiency of the heart leading to heterogenous changes in cardiac output. Changes in the pressure gradient for venous return and cardiac output, scaled by the change in MAP, were positively correlated (r2 = 0.88, P < 0.001). Changes in the mean systemic filling pressure analogue and heart pump efficiency were negatively correlated (r2 = 0.57, P < 0.001) while no correlation was found between changes in MAP and heart pump efficiency.We conclude that hemodynamic changes induced by vasopressor therapy are inadequately represented by the change in MAP alone despite its common use as a clinical endpoint. The more comprehensive analysis applied in this review illustrates how vasopressor administration may be optimized.

Volume status and volume responsiveness in postoperative cardiac surgical patients: An observational, multicentre cohort study.

The best strategy to identify patients in whom fluid loading increases cardiac output (CO) following cardiac surgery remains debated. This study examined the utility of a calculated mean systemic filling pressure analogue (Pmsa ) and derived variables to explain the response to a fluid bolus. The Pmsa was calculated using retrospective, observational cohort data in the early postoperative period between admission to the intensive care unit and extubation within 6hours. The venous return pressure gradient (VRdP) was calculated as Pmsa -central venous pressure. Concurrent changes induced by a fluid bolus in the ratio of the VRdP over Pmsa , the volume efficiency (Evol ), were studied to assess fluid responsiveness. Changes between Pmsa and derived variables and CO were analysed by Wilcoxon rank-sum test, hierarchial clustering and multiple linear regression. Data were analysed for 235 patients who received 489 fluid boluses. The Pmsa increased with consecutive fluid boluses (median difference [range] 1.3 [0.5-2.4] mmHg, P=.03) with a corresponding increase in VRdP (median difference 0.4 [0.2-0.6] mmHg, P=.04). Hierarchical cluster analysis only identified Evol and the change in CO within one cluster. The multiple linear regression between Pmsa and its derived variables and the change in CO (overall r2 =.48, P<.001) demonstrated the best partial regression between the continuous change in CO and the concurrent Evol (r=.55, P<.001). The mean systemic filling Pmsa enabled a comprehensive interpretation of fluid responsiveness with volume efficiency useful to explain the change in CO as a continuous phenomenon.

Pressure Gradient for Venous Return in Predicting Fluid Responsiveness in Patients Undergoing Laparoscopic Surgery

Pressure Gradient for Venous Return in Predicting Fluid Responsiveness in Patients Undergoing Laparoscopic Surgery

Heart-lung interactions during mechanical ventilation: the basics.

The hemodynamic effects of mechanical ventilation can be grouped into three clinically relevant concepts. First, since spontaneous ventilation is exercise. In patients increased work of breathing, initiation of mechanical ventilatory support may improve O2 delivery because the work of breathing is reduced. Second, changes in lung volume alter autonomic tone, pulmonary vascular resistance, and at high lung volumes compress the heart in the cardiac fossa similarly to cardiac tamponade. As lung volume increases so does the pressure difference between airway and pleural pressure. When this pressure difference exceeds pulmonary artery pressure, pulmonary vessels collapse as they pass form the pulmonary arteries into the alveolar space increasing pulmonary vascular resistance. Hyperinflation increases pulmonary vascular resistance impeding right ventricular ejection. Anything that over distends lung units will increase their vascular resistance, and if occurring globally throughout the lung, increase pulmonary vascular resistance. Decreases in end-expiratory lung volume cause alveolar collapse increases pulmonary vasomotor tone by the process of hypoxic pulmonary vasoconstriction. Recruitment maneuvers that restore alveolar oxygenation without over distention will reduce pulmonary artery pressure. Third, positive-pressure ventilation increases intrathoracic pressure. Since diaphragmatic descent increases intra-abdominal pressure, the decrease in the pressure gradient for venous return is less than would otherwise occur if the only change were an increase in right atrial pressure. However, in hypovolemic states, it can induce profound decreases in venous return. Increases in intrathoracic pressure decreases left ventricular afterload and will augment left ventricular ejection. In patients with hypervolemic heart failure, this afterload reducing effect can result in improved left ventricular ejection, increased cardiac output and reduced myocardial O2 demand. This brief review will focus primarily on mechanical ventilation and intrathoracic pressure as they affect right and left ventricular function and cardiac output.

Exercise intolerance in heart failure with preserved ejection fraction: time to scrutinize diuretic therapy?

Exercise intolerance in heart failure with preserved ejection fraction: time to scrutinize diuretic therapy?

The right ventricle: interaction with the pulmonary circulation.

The primary role of the right ventricle (RV) is to deliver all the blood it receives per beat into the pulmonary circulation without causing right atrial pressure to rise. To the extent that it also does not impede left ventricular (LV) filling, cardiac output responsiveness to increased metabolic demand is optimized. Since cardiac output is a function of metabolic demand of the body, during stress and exercise states the flow to the RV can vary widely. Also, instantaneous venous return varies widely for a constant cardiac output as ventilatory efforts alter the dynamic pressure gradient for venous return. Normally, blood flow varies with minimal changes in pulmonary arterial pressure. Similarly, RV filling normally occurs with minimal increases in right atrial pressure. When pulmonary vascular reserve is compromised RV ejection may also be compromised, increasing right atrial pressure and limiting maximal cardiac output. Acute increases in RV outflow resistance, as may occur with acute pulmonary embolism, will cause acute RV dilation and, by ventricular interdependence, markedly decreased LV diastolic compliance, rapidly spiraling to acute cardiogenic shock and death. Treatments include reversing the causes of pulmonary hypertension and sustaining mean arterial pressure higher than pulmonary artery pressure to maximal RV coronary blood flow. Chronic pulmonary hypertension induces progressive RV hypertrophy to match RV contractility to the increased pulmonary arterial elastance. Once fully developed, RV hypertrophy is associated with a sustained increase in right atrial pressure, impaired LV filling, and decreased exercise tolerance. Treatment focuses on pharmacologic therapies to selectively reduce pulmonary vasomotor tone and diuretics to minimize excessive RV dilation. Owning to the irreversible nature of most forms of pulmonary hypertension, when the pulmonary arterial elastance greatly exceeds the adaptive increase in RV systolic elastance, due to RV dilation, progressive pulmonary vascular obliteration, or both, end stage cor pulmonale ensues. If associated with cardiogenic shock, it can effectively be treated only by artificial ventricular support or lung transplantation. Knowing how the RV adapts to these stresses, its sign posts, and treatment options will greatly improve the bedside clinician’s ability to diagnose and treat RV dysfunction.

Peripheral Venous Pressure as an Indicator of Preload Responsiveness During Volume Resuscitation from Hemorrhage.

Fluid resuscitation of hypovolemia presumes that peripheral venous pressure (PVP) increases more than right atrial pressure (RAP), so the net pressure gradient for venous return (PVP-RAP) rises. However, the heart and peripheral venous system function under different compliances that could affect their respective pressures during fluid infusion. In a porcine model of hemorrhage resuscitation, we examined whether RAP increases more than PVP, thereby reducing the venous return pressure gradient and blood flow. Anesthetized pigs (n = 8) were bled to a mean arterial blood pressure of 40 mm Hg and resuscitated with stored blood and albumin for pulmonary artery occlusion pressures (PAOPs) of 5, 10, 15, and 20 mm Hg. Venous pressures, inferior vena cava blood flow (ultrasonic flowprobe), and left ventricular diastolic compliance (Doppler echocardiography) were measured. Stroke volume variability was calculated. With volume resuscitation, the slope of RAP exceeded PVP (P ≤ 0.0001) when PAOP is 10 to 20 mm Hg, causing the pressure gradient for venous return to progressively decrease. Inferior vena cava blood flow did not further increase after PAOP > 10 mm Hg. The E/e' ratio increased (P = 0.001) during resuscitation indicating reduced diastolic compliance. A significant curvilinear relationship was found between PVP and stroke volume variability (R = 0.62; P < 0.001), where fluid responders had PVP < 15 mm Hg. Fluid resuscitation above a PAOP 10 mm Hg reduces myocardial compliance and reduces the venous return pressure gradient. The hemodynamic response to fluid resuscitation becomes limited by diastolic properties of the heart. PVP measurement during hemorrhage resuscitation may predict fluid responsiveness and nonresponsiveness.

Central venous pressure: we need to bring clinical use into physiological context.

The place of central venous pressure (CVP) measurement in acute care has been questioned during the past decade. We reviewed its physiological importance, utility and clinical use among anaesthetists and intensivists. A literature search using the PubMed, Cochrane, Scopus and Web of Science databases was performed in regard to details of the physiology, measurement and interpretation of CVP. A questionnaire was conducted among members of the European Society of Intensive Care Medicine concerning knowledge and uses of CVP. Aligning pressure transducers to the phlebostatic axis was handled inadequately. The unsuitability of CVP to assess the intravascular volume state was generally recognised by clinicians. Still, many used CVP to guide volume resuscitation in the absence of a cardiac output monitor, while the literature positioned CVP as a useful haemodynamic variable only in the expanded context of being one determinant of the driving pressure for venous return and hence cardiac output. The correct measurement of CVP is pivotal to its proper clinical application. This relates to defining the pressure gradient for venous return and heart efficiency. The clinical appreciation of CVP should be restored by educational efforts of its physiological context.

Applying mean systemic filling pressure to assess the response to fluid boluses in cardiac post-surgical patients.

To evaluate an analogue of mean systemic filling pressure (P(msa)) and derived variables to quantitatively assess the effectiveness of volume expansion in increasing cardiac output. Sixty-one cardiac post-surgical patients were studied and 107 fluid boluses were captured. Cardiac output, mean arterial pressure and right atrial pressure were recorded with P msa before and after a bolus fluid. An increase in cardiac output greater than 10 % following a fluid bolus defined a patient as a responder. Cardiac power (i.e. the product of arterial pressure and cardiac output) and P(msa) to right atrial pressure gradient (i.e. the driving pressure for venous return and hence cardiac output) were evaluated to assess the efficiency of volume expansion to increase cardiac output. Cardiac power relative to P(msa) (CP(vol)), its dynamic changes and the dynamic changes in P msa-right atrial pressure gradient relative to the P(msa) change (E(vol)) were investigated. CP(vol) was lower and E(vol) was higher in responders vs. non-responders. Furthermore, in patients receiving a second fluid bolus, E(vol) correlated with the degree of increase in cardiac output. Multivariate regression analysis identified both CP(vol) and E(vol) as independent variables associated with volume responsiveness. Using an algorithm to derive a mean systemic filling pressure analogue, cardiac power and dynamic measures of the venous return pressure gradient relative to the mean systemic filling pressure provided an assessment of the efficiency of volume expansion in post-surgical cardiac patients.

Case Scenario

Case Scenario

Bedside assessment of passive leg raising effects on venous return

Passive leg raising (PLR) provides a reversible fluid-loading challenge and can be used to predict fluid responsiveness. The amount of blood volume recruited by this maneuver called stressed volume (Vs) is unknown. The present study aims to assess the quantitative effects of passive leg raising on venous return at bedside. We conducted a prospective interventional study. Nine mechanically ventilated postoperative cardiac surgery patients with preserved left ventricular function were enrolled. Cardiac output (CO) was continuously monitored by PiCCO™ via the pulse contour method. Ten second intervals of inspiratory breath holding at four plateau pressures (5, 15, 25 and 35cm H(2)O) were performed to measure the relationship between blood flow (CO) and central venous pressure (CVP). These were used to determine mean systemic filling pressure (Pmsf) and Vs. Patients were studied at three successive steps: semirecumbent position, after PLR and back in the semirecumbent position after volume expansion (VE). Similar to VE, PLR significantly increased Pmsf from 19.7 (17.0-22.6) mmHg at baseline to 22.0 (18.5-27.8) mmHg (p <0.05). CO increased 11.1% (9.5-20) with PLR and 14.8% (4.2-19.9) with VE. Venous return resistance was unchanged throughout the three conditions, whereas the the pressure gradient for venous return (Pmsf-CVP) increased during PLR (p=0.058) and during VE (p < 0.05). Baseline circulatory compliance was 1.14 (0.52-2.65)mlmmHg(-1)kg(-1). Vs increased to 3.5 (1.1-3.9) mlkg(-1) with PLR. The effect of transient hemodynamic changes on venous return induced by passive leg raising can be directly measured in intensive care patients using inspiratory-hold procedures. This technique makes quantification of PLR feasible and could be used clinically to assess fluid responsiveness.

Bedside assessment of mean systemic filling pressure

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. 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. 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.

Control of Cardiac Output

Abstract Although cardiac output is measured as the flow of blood from the left ventricle into the aorta, the system that controls cardiac output includes many other components besides the heart itself. The heart’s rate of output cannot exceed the rate of venous return to it, and therefore, the factors governing venous return are primarily responsible for control of output from the heart. Venous return is affected by its pressure gradient and resistance to flow throughout the vascular system. The pressure gradient for venous return is a function of several factors including the blood volume flowing through the system, the unstressed vascular volume of the circulatory system, its capacitance, mean systemic pressure, and right atrial pressure. Resistance to venous return is the sum of total vascular resistance from the aortic valve to the right atrium. The sympathetic nervous system and vasoactive circulating hormones affect short-term resistance, whereas local tissue blood flow autoregulatory mechanisms ar...

Inspiratory Increases in Systolic Blood Pressure (“Delta-up”) and Pulse Pressure Are Not Equivalent

Inspiratory Increases in Systolic Blood Pressure (“Delta-up”) and Pulse Pressure Are Not Equivalent

Venous hemodynamic responses to acute temperature increase in the rainbow trout (Oncorhynchus mykiss)

Many ectotherms regularly experience considerable short-term variations in environmental temperature, which affects their body temperature. Here we investigate the cardiovascular responses to a stepwise acute temperature increase from 10 to 13 and 16 degrees C in rainbow trout (Oncorhynchus mykiss). Cardiac output increased by 20 and 31% at 13 and 16 degrees C, respectively. This increase was entirely mediated by an increased heart rate (fH), whereas stroke volume (SV) decreased significantly by 20% at 16 degrees C. The mean circulatory filling pressure (MCFP), a measure of venous capacitance, increased with temperature. Central venous pressure (Pven) did not change, whereas the pressure gradient for venous return (MCFP-Pven) was significantly increased at both 13 and 16 degrees C. Blood volume, as measured by the dilution of 51Cr-labeled red blood cells, was temperature insensitive in both intact and splenectomized trout. This study demonstrates that venous capacitance in trout decreases, but cardiac filling pressure as estimated by Pven does not change when cardiac output increases during an acute temperature increase. SV was compromised as fH increased with temperature. The decreased capacitance likely serves to prevent passive pooling of blood in the venous periphery and to maintain cardiac filling pressure and a favorable pressure gradient for venous return.

Cardiovascular Issues in Respiratory Care

The hemodynamic effects of ventilation are complex but can be grouped under four clinically relevant concepts. First, spontaneous ventilation is exercise, and critically ill patients may not withstand the increased work of breathing. Initiation of mechanical ventilatory support will improve oxygen delivery to the remainder of the body by decreasing oxygen consumption. To the extent that mixed venous oxygen also increases, Pao(2) will increase without any improvement in gas exchange. Similarly, weaning from mechanical ventilatory support is a cardiovascular stress test. Patients who fail to wean also manifest cardiovascular insufficiency during the failed weaning attempts. Improving cardiovascular reserve or supplementing support with inotropic therapy may allow patients to wean from mechanical ventilation. Second, changes in lung volume alter autonomic tone and pulmonary vascular resistance (PVR), and at high lung volumes compress the heart in the cardiac fossa. Hyperinflation increases PVR and pulmonary artery pressure, impeding right ventricular ejection. Decreases in lung volume induce alveolar collapse and hypoxia, stimulating an increased pulmonary vasomotor tone by the process of hypoxic pulmonary vasoconstriction. Recruitment maneuvers, positive end-expiratory pressure, and continuous positive airway pressure may reverse hypoxic pulmonary vasoconstriction and reduce pulmonary artery pressure. Third, spontaneous inspiration and spontaneous inspiratory efforts decrease intrathoracic pressure (ITP). Since diaphragmatic descent increases intra-abdominal pressure, these combined effects cause right atrial pressure inside the thorax to decrease but venous pressure in the abdomen to increase, markedly increasing the pressure gradient for systemic venous return. Furthermore, the greater the decrease in ITP, the greater the increase in left ventricular (LV) afterload for a constant arterial pressure. Mechanical ventilation, by abolishing the negative swings in ITP, will selectively decrease LV afterload, as long as the increases in lung volume and ITP are small. Finally, positive-pressure ventilation increases ITP. Since diaphragmatic descent increases intra-abdominal pressure, the decrease in the pressure gradient for venous return is less than would otherwise occur if the only change were an increase in right atrial pressure. However, in hypovolemic states, positive-pressure ventilation can induce profound decreases in venous return. Increases in ITP decrease LV afterload and will augment LV ejection. In patients with hypervolemic heart failure, this afterload reducing effect can result in improved LV ejection, increased cardiac output, and reduced myocardial oxygen demand.

Cardiac preload and venous return in swimming sea bass (Dicentrarchus labraxL.)

Cardiac preload (central venous pressure, P(CV), mean circulatory filling pressure (MCFP), dorsal aortic blood pressure (P(DA)) and relative cardiac output (Q) were measured in sea bass (Dicentrarchus labrax) at rest and while swimming at 1 and 2 BL s(-1). MCFP, an index of venous capacitance and the upstream venous pressure driving the return of venous blood to the heart, was measured as the plateau in Pcv during ventral aortic occlusion. Compared with resting values, swimming at 1 and 2 BL s(-1) increased Q (by 15+/-1.5 and 38+/-6.5%, respectively), P(CV) (from 0.11+/-0.01 kPa to 0.12+/-0.01 and 0.16+/-0.02 kPa, respectively), MCFP (from 0.27+/-0.02 kPa to 0.31+/-0.02 and 0.40+/-0.04 kPa, respectively) and the calculated pressure gradient for venous return (DeltaP(V), from 0.16+/-0.01 kPa to 0.18+/-0.02 and 0.24+/-0.02 kPa, respectively), but not P(DA). In spite of an increased preload, the increase in Q was exclusively mediated by an increased heart rate (f(H), from 80+/-4 beats min(-1) to 88+/-4 and 103+/-3 beats min(-1), respectively), and stroke volume (Vs) remained unchanged. Prazosin treatment (1 mg kg(-1) Mb) abolished pressure and flow changes during swimming at 1 BL s(-1), but not 2 BL s(-1), indicating that other control systems besides an alpha-adrenoceptor control are involved. This study is the first to address the control of venous capacitance in swimming fish. It questions the generality that increased Q during swimming is regulated primarily through Vs and shows that an increased cardiac filling pressure does not necessarily lead to an increased Vs in fish, but may instead compensate for a reduced cardiac filling time.