Vascular Waterfall Research Articles

Considerations on static pressure gradients in closed circulatory systems.

Siphons are devices that transport liquids uphill between two containers. It has been proposed that a siphon principle operates in closed circulatory systems, as best exemplified by the circulation of blood in mammals. This principle is supposed to ensure that no additional work is necessary to pump blood above the level of the heart, and that there is no gravitational static pressure gradient in the column of blood. The first statement is correct, while we demonstrate that, ignoring hydraulic resistance to blood flow, the static pressure gradient is equal to the hydrostatic gradient in a siphon model of blood circulation, although the details of the proof do not depend on the geometry of the circulatory system and the proof can be trivially extended to other models such as a vascular waterfall. This implies that the controversy over the siphon principle has no implications for the description of blood circulation, and that mechanisms such as the "baffle," which some authors have appealed to in order to obtain the expected gradient, are not necessary. In our discussion, we also discuss empirical data that appear to provide additional verification of our results, as well as several everyday occurrences that provide additional support.

Effect of norepinephrine on the vascular waterfall and tissue perfusion in vasoplegic hypotensive patients: a prospective, observational, applied physiology study in cardiac surgery

BackgroundNorepinephrine is a commonly used drug for treating vasoplegic acute circulatory failure in ICU. The prediction of norepinephrine macro- and micro-circulatory response is complicated by its uneven receptors’ distribution between the arterial and the venous structures, and by the presence of a physiological vascular waterfall (VW) that disconnects the arterial and the venous circulation in two pressure systems. The objectives of this study were to describe the VW in patients with arterial hypotension due to vasodilatory circulatory shock, and its behavior according to its response to norepinephrine infusion.MethodsA prospective, observational, bi-centric study has included adult patients, for whom the physician decided to initiate norepinephrine during the six first hours following admission to the ICU after cardiac surgery, and unresponsive to a fluid challenge. The mean systemic pressure (MSP) and the critical closing pressure (CCP) were measured at inclusion and after norepinephrine infusion.ResultsThirty patients were included. Norepinephrine increased arterial pressure and total peripheral resistances in all cohort. The cohort was dichotomized as VW responders (patients with a change of VW over the least significant change (≥ 93% increase in VW)), and as VW non-responders. In 19 (63%) of the 30 patients, VW increased from 3.47 [− 14.43;7.71] mmHg to 43.6 [25.8;48.1] mmHg, p < 0.001) with norepinephrine infusion, being classified as VW responders. The VW responders improved cardiac index (from 1.8 (0.6) L min−1 m−2 to 2.2 (0.5) L min−1 m−2, p = 0.002), capillary refill time (from to 4.2 (1.1) s to 3.1 (1) s, p = 0.006), and pCO2 gap (from 9 [7;10] mmHg to 6 [4;8] mmHg, p = 0.04). No baseline parameters were able to predict the VW response to norepinephrine. In comparison, VW non-responders did not significantly change the VW (from 5 [-5;16] mmHg to -2 [-12;15] mmHg, p = 0.17), cardiac index (from 1.6 (0.3) L min−1 m−2 to 1.8 (0.4) L min−1 m−2, p = 0.09) and capillary refill time (from 4.1 (1) s to 3.7 (1.4), p = 0.44).ConclusionsIn post-cardiac surgery patients with vasoplegic arterial hypotension, the vascular waterfall is low. Norepinephrine did not systematically restore the vascular waterfall. Increase of the vascular waterfall was associated with an improvement of laboratory and clinical parameters of tissue perfusion.

Esmolol response in septic shock patients in relation to vascular waterfall phenomenon measured by critical closure pressure and mean systemic filling pressure: a prospective observational study

BackgroundBedside measurements of critical closure pressure (Pcc) and mean systemic circulation filling pressure (Pmsf) were utilized to evaluate the response to esmolol in septic shock patients, in relation to the vascular waterfall phenomenon and body oxygen supply and demand.MethodsThis prospective observational self-controlled study included patients with septic shock, newly admitted to the intensive care unit, between August 2019 and January 2021. Pcc and Pmsf, along with the heart rate and other hemodynamic indicators were observed and compared before and 1 h after esmolol IV infusion.ResultsAfter 24 h of initial hemodynamic optimization, 56 patients were finally enrolled. After start of esmolol infusion, patients had a significant decrease in cardiac index (CI) (4.0 vs. 3.3 L/min/m2, P < 0.001), a significant increase in stroke index (SI) (34.1 vs. 36.6 mL/m2, P < 0.01), and a significant decrease in heart rate (HR) (116.8 vs. 90.6 beats/min, P < 0.001). After 1 h of treatment with esmolol, patients had a significant increase in Pcc (31.4 vs. 36.7 mmHg, P < 0.01). The difference between Pcc and Pmsf before and after treatment was statistically different (4.0 vs. 10.0 mmHg, P < 0.01). After heart rate control with esmolol, the patients had a significant increase in the body circulation vascular resistance indices (RIs) (15.14 vs. 18.25 mmHg/min/m2/L, P < 0.001). There was an increase in ScvO2 in patients after treatment with esmolol, but the difference was not statistically significant (68.4% vs. 69.8%, P > 0.05), while Pcv-aCO2 was significantly lower (6.3 vs. 4.9 mmHg, P < 0.001) and patients had a significant decrease in blood lactate levels (4.0 vs. 3.6 mmol/L, P < 0.05).ConclusionPatients with septic shock whose heart rate is greater than 95 beats/min after hemodynamic optimization were treated with esmolol, which could effectively control heart rate and reduce CI, as well as improve Pcc and increase the difference between Pcc and Pmsf (known as “vascular waterfall” phenomenon), without affecting MAP, CVP, Pmsf and arteriovenous vascular resistance, and improve the balance of oxygen supply and demand in the body.

Dynamic Arterial Elastance Is Associated With the Vascular Waterfall in Patients Treated With Norepinephrine: An Observational Study.

Introduction: It has been suggested that dynamic arterial elastance (Eadyn) can predict decreases in arterial pressure in response to changing norepinephrine levels. The objective of this study was to determine whether Eadyn is correlated with determinants of the vascular waterfall [critical closing pressure (CCP) and systemic arterial resistance (SARi)] in patients treated with norepinephrine.Materials and Methods: Patients treated with norepinephrine for vasoplegia following cardiac surgery were studied. Vascular and flow parameters were recorded immediately before the norepinephrine infusion and then again once hemodynamic parameters had been stable for 15 min. The primary outcomes were Eadyn and its associations with CCP and SARi. The secondary outcomes were the associations between Eadyn and vascular/flow parameters.Results: At baseline, all patients were hypotensive with Eadyn of 0.93 [0.47;1.27]. Norepinephrine increased the arterial blood pressure, cardiac index, CCP, total peripheral resistance (TPRi), arterial elastance, and ventricular elastance and decreased Eadyn [0.40 (0.30;0.60)] and SARi. Eadyn was significantly associated with arterial compliance (CA), CCP, and TPRi (p < 0.05).Conclusion: In patients with vasoplegic syndrome, Eadyn was correlated with determinants of the vascular waterfall. Eadyn is an easy-to-read functional index of arterial load that can be used to assess the patient’s macro/microcirculatory status.Clinical Trial Registration: ClinicalTrials.gov #NCT03478709.

The caval sphincter in cetaceans and its predicted role in controlling venous flow during a dive.

A sphincter on the inferior vena cava can protect the heart of a diving mammal from overload when elevated abdominal pressures increase venous return, yet sphincters are reported incompetent or absent in some cetacean species. We previously hypothesized that abdominal pressures are elevated and pulsatile in fluking cetaceans, and that collagen is deposited on the diaphragm according to pressure levels to resist deformation. Here, we tested the hypothesis that cetaceans generating high abdominal pressures need a more robust sphincter than those generating low pressures. We examined diaphragm morphology in seven cetacean and five pinniped species. All odontocetes had morphologically similar sphincters despite large differences in collagen content, and mysticetes had muscle that could modulate caval flow. These findings do not support the hypothesis that sphincter structure correlates with abdominal pressures. To understand why a sphincter is needed, we simulated the impact of oscillating abdominal pressures on caval flow. Under low abdominal pressures, simulated flow oscillated with each downstroke. Under elevated pressures, a vascular waterfall formed, greatly smoothing flow. We hypothesize that cetaceans maintain high abdominal pressures to moderate venous return and protect the heart while fluking, and use their sphincters only during low-fluking periods when abdominal pressures are low. We suggest that pinnipeds, which do not fluke, maintain low abdominal pressures. Simulations also showed that retrograde oscillations could be transmitted upstream from the cetacean abdomen and into the extradural veins, with potentially adverse repercussions for the cerebral circulation. We propose that locomotion-generated pressures have influenced multiple aspects of the cetacean vascular system.

The β-Blocker Esmolol Restores the Vascular Waterfall Phenomenon After Acute Endotoxemia*

A vascular waterfall occurs when the critical closing pressure is greater than the mean systemic filling pressure. Because the waterfall phenomenon likely exists in the microcirculation, β1-receptor blockers such as esmolol could have some effect on microcirculation and vascular waterfall. To determine whether a vascular waterfall exists during septic shock and to assess the effects of vasopressors and β-blockers on vascular waterfall. Sixteen mongrel dogs were mounted with ultrasonic flow probes to measure renal blood flow. The hemodynamic variables of 16 animals were measured at baseline, after induction of acute endotoxemia; then, they underwent volume expansion, and norepinephrine was used to achieve baseline. After achieving septic myocardial depression, the animals were randomly divided into two groups (esmolol vs control groups) after reaching septic myocardial depression. There was a pressure gap of 41.9 ± 13.9 mm Hg between the arterial critical closing pressure and the mean systemic filling pressure, indicating that a vascular waterfall was present under baseline conditions. Endotoxemia caused a decrease in cardiac output, mean arterial pressure, and critical closing pressure. Endotoxemia also caused the vascular waterfall to disappear. Neither volume expansion nor norepinephrine had any effect on the vascular waterfall. Esmolol infusion restored the vascular waterfall effect following endotoxemia and resuscitation. The 24-hour survival was 75% in the esmolol group versus 12.5% in controls (p = 0.041). Vascular pressure gradients in renal vasculature suggest the presence of a vascular waterfall at baseline. Although this phenomenon disappeared in endotoxemic dogs, it could be restored with β-blocker therapy (esmolol).

Effect of PEEP, blood volume, and inspiratory hold maneuvers on venous return.

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.

Where is the vascular waterfall in septic shock?

An evaluation of a recent study by Asfar P, Meziani F, Hamel J-F, et al. High versus low blood-pressure target in patients with septic shock. N Engl J Med 2014;370:1583-1593.

研究 フィブリノゲン分解酵素(DF-521)の大腿動脈圧流量関係に及ぼす効果

研究 フィブリノゲン分解酵素(DF-521)の大腿動脈圧流量関係に及ぼす効果

Determination of Vascular Waterfall Phenomenon by Bedside Measurement of Mean Systemic Filling Pressure and Critical Closing Pressure in the Intensive Care Unit

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. 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. 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. 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.

Understanding Coronary Blood Flow

Fick’s principle states that oxygen consumption of an organ or organism is equal to the product of blood flow and oxygen extraction from the blood. Among all organs, the heart is unique in that oxygen extraction is constantly close to maximal. Thus, the only way that this metabolically demanding organ can increase oxygen consumption is by increasing coronary blood flow. In this aspect of oxygen delivery, the heart also is unique because most flow occurs in diastole instead of in systole. In other organs, blood flows down a pressure gradient from its arterial source through the resistance of the arterioles into the capillary bed and thence venous return. In the heart, the compression of the vasculature by its surrounding muscle during systole impedes flow so that while the pressure head for flow is maximum in systole, flow is maximum in diastole. Thus, a simple “vascular waterfall” model in which flow moves from highest to lowest pressure does not fully explain observed myocardial flow phenomena. Article p 1768 In this week’s Circulation , Davies et al1 used computer analysis of recordings of blood flow and pressure to detect and quantify intracoronary …

Teaching the effects of gravity and intravascular and alveolar pressures on the distribution of pulmonary blood flow using a classic paper by West et al.

"Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures" by J. B. West, C. T. Dollery, and A. Naimark (J Appl Physiol 19: 713-724, 1964) is a classic paper, although it has not yet been included in the Essays on the American Physiological Society Classic Papers Project (http://www.the-aps.org/publications/classics/). This is the paper that originally described the "zones of the lung." The final figure in the paper, which synthesizes the results and discussion, is now seen in most textbooks of physiology or respiratory physiology. The paper is also a model of clear, concise writing. The paper and its final figure can be used to teach or review a number of physiological concepts. These include the effects of gravity on pulmonary blood flow and pulmonary vascular resistance; recruitment and distention of pulmonary vessels; the importance of the transmural pressure on the diameter of collapsible distensible vessels; the Starling resistor; the interplay of the pulmonary artery, pulmonary vein, and alveolar pressures; and the vascular waterfall. In addition, the figure can be used to generate discovery learning and discussion of several physiological or pathophysiological effects on pulmonary vascular resistance and the distribution of pulmonary blood flow.

Instantaneous diastolic pressure–flow relationship in arterial coronary bypass grafts

The objective of this study was to describe the diastolic pressure-flow relationship and to assess critical occlusion pressure in arterial coronary bypass grafts in human beings. Fifteen patients were studied following elective surgical coronary artery bypass grafting. Flow in the left internal mammary artery bypass to the left anterior descending artery was measured and simultaneously, aortic pressure, coronary sinus pressure and left ventricular end-diastolic pressure were recorded. The zero-flow pressure intercept as a measure of critical occlusion pressure was extrapolated from the linear regression analysis of the instantaneous diastolic pressure-flow relationship. Mean diastolic flow was 46 +/- 17 mL min(-1), mean diastolic aortic pressure was 60.5 +/- 10.0 mmHg. Diastolic blood flow was linearly related to the respective aortic pressure in all patients (R-values 0.7-0.99). The regression lines had a mean slope of 2.1 +/- 1.2 mL min(-1) mmHg(-1). Mean critical occlusion pressure was 32.3 +/- 9.9 mmHg and exceeded mean coronary sinus pressure and mean left ventricular end-diastolic pressure by factors of 3.1 and 2.6, respectively. Our data demonstrate the presence of a vascular waterfall phenomenon in the coronary circulation after internal mammary artery bypass grafting. Critical occlusion pressure in arterial grafts considerably exceeds coronary sinus pressure as well as left ventricular end-diastolic pressure and should thus be used as the effective downstream pressure when calculating coronary perfusion pressure. Our data further suggest that the slope of diastolic pressure-flow relationships provides a more rational approach to assess regional coronary vascular resistance than conventional calculations of coronary vascular resistance.

Modeling of the Coronary Circulatory System

The dynamics of the coronary system is complicated by its dependence on the mechanical properties of the coronary vessels, the anatomical distribution of the vasculature, the biochemical and neurohormonal regulation, and the effect of myocardial contraction. Several types of coronary system models were proposed, focusing on different aspects of coronary system behavior and supported by different animal experiment methodologies. The lumped models were based on well-controlled coronary pressure–flow measurement and simplified assumptions. They are probably most useful for interpreting hemodynamic data measured in modern catheterizaton labs. Anatomical models, with the advancement in morphometric research, coronary angiography, and video densitometry, provided branching pattern, geometric distribution, and distensibility of coronary vessels. Mathematical description based on vascular waterfall theory, intramyocardial pump model, and time varying elastance concept provided some explanation of the interaction between the coronary system and myocardial contraction. More accurate models would include intramyocardial pressure, microcirculatory hemodynamics, coronary flow regulation, and myocardial oxygen supply and consumption. The combination of different models, may lead to a more comprehensive understanding of the coronary system.

The siphon controversy counterpoint: the brain need not be “baffling”

The application of siphon principles to the cerebral circulation has engendered a surprising amount of controversy (1–3, 11, 19, 22, 23). The reluctance to apply siphon principles to the cerebral circulation probably stems more from its inescapable, but counterintuitive, corollary: if the

The physiological basis of arterial pressure variation during positive-pressure ventilation

The aim of this communication is to present an overview of the physiological basis of arterial pressure variations during positive-pressure ventilation. The review describes the effects of the mechanical breath on the right and left ventricles, and in particular the vascular waterfall effect and the reduction in venous return and the inspiratory increase in LV preload. A better understanding of the hemodynamic consequences of mechanichal ventilation will help the reader to correctly interpret arterial pressure variations and apply their derived parameters into clinical decision-making.

Microvascular pressure measurement reveals a coronary vascular waterfall in arterioles larger than 110 μm

Pressure-flow relationships at the entrance of the coronary circulation in the diastolic myocardium exhibit a zero-flow pressure intercept (P(int)). We tested whether this intercept is the same throughout the vascular bed. Microvascular pressure-flow relationships were therefore measured in vessels of various sizes of the maximally dilated vasculature of perfused unstimulated papillary muscle using the servo-null technique. From these relationships, P(int) were calculated with nonlinear regression. The P(int) at the level of the septal artery (diameter, 150-250 microm) was 23.2 +/- 4.4 cmH2O (n = 12). In arterioles with a diameter range between 24 and 110 microm, P(int) was 1.7 +/- 0.5 cmH2O (n = 6, P < 0.01), significantly lower than in the septal artery but significantly higher than zero, and not dependent on vessel size. In venules with the same diameters, P(int) was 1.1 +/- 1.1 cmH2O (n = 4), which was not different from zero. We conclude that, in the dilated vascular bed of the papillary muscle, two vascular waterfalls are found. The first waterfall is located in arterioles between 150 and 110 microm. The second waterfall is probably located in the small postcapillary venules.

Spatial interaction between tissue pressure and skeletal muscle perfusion during contraction

The vascular waterfall theory attributes decreased muscle perfusion during contraction to increased intramuscular pressure ( P IM) and concomitant increase in venous resistance. Although P IM is distributed during contractions, this theory does not account for heterogeneity. This study hypothesises that pressure heterogeneity could affect the interaction between P IM rise and perfusion. Regional tissue perfusion during submaximum (100 kPa) tetanic contraction is studied, using a finite element model of perfused contracting skeletal muscle. Capillary flow in muscles with one proximal artery and vein (SIM 1) and with an additional distal artery and vein (SIM 2) is compared. Blood flow and pressures at rest and P IM during contraction (∼25 kPa maximally) are similar between simulations, but capillary flow and venous pressure differ. In SIM 2, venous pressure and capillary flow correspond to P IM distribution, whereas capillary flow in SIM 1 is less than 10% of flow in SIM 2, in the muscle half without draining vein. This difference is caused by a high central P IM, followed by central venous pressure rise, in agreement with the waterfall theory. The high central pressure (SIM 1), obstructs outflow from the distal veins. Distal venous pressure rises until central blood pressure is reached, although local P IM is low. Adding a distal vein (SIM 2) restores the perfusion. It is concluded that regional effects contribute to the interaction between P IM and perfusion during contraction. Unlike stated by the vascular waterfall theory, venous pressure may locally exceed P IM. Although this can be explained by the principles of this theory, the theory does not include this phenomenon as such.

Influence of increased abdominal pressure on steady-state cardiac performance.

The effect of steady-state increases in abdominal pressure (Pab) on cardiac performance was studied in seven acutely instrumented swine with pneumoperitoneum (PP). The animal was placed on volume-preset ventilation, and PP was created by air insufflation. Cardiac output (CO), right atrial (Pra), left atrial (Pla), pericardial (Ppe), and abdominal inferior vena cava pressures (Pivc) were measured while Pab was increased from baseline to 7.5, 15, and 30 mmHg (PP7.5, PP15, and PP30, respectively). Cardiac function curves of the right and left ventricle (RV and LV, respectively) were compared between baseline and PP30. CO presented biphasic changes, with an inital slight increase at PP7.5 followed by a fall at PP30. A significant discrepancy was observed between Pra and Pivc at PP15 and PP30, consistent with development of a "vascular waterfall." Transmural Pla (Pla - Ppe) showed parallel changes with CO, whereas transmural Pra (Pra - Ppe) exhibited a sustained increase. The RV cardiac-function curve was more depressed than was that of the LV at PP30; this suggests an increased RV afterload produced by the elevated airway pressure. These results support the hypothesis that our previously proposed concept of abdominal vascular zone conditions (M. Takata, R. A. Wise, and J. L. Robotham. J. Appl. Physiol. 69: 1961-1972, 1990) is also applicable to steady-state hemodynamic analyses. The abdominal zones appear to play an important role in determining CO, with increases in Pab, by modulating systemic venous return and the LV preload. Simultaneous measurements of Pra and Pivc may provide useful information in the hemodynamic care of patients with elevated Pab.

Finite-element simulation of blood perfusion in muscle tissue during compression and sustained contraction.

Mechanical interaction between tissue stress and blood perfusion in skeletal muscles plays an important role in blood flow impediment during sustained contraction. The exact mechanism of this interaction is not clear, and experimental investigation of this mechanism is difficult. We developed a finite-element model of the mechanical behavior of blood-perfused muscle tissue, which accounts for mechanical blood-tissue interaction in maximally vasodilated vasculature. Verification of the model was performed by comparing finite-element results of blood pressure and flow with experimental measurements in a muscle that is subject to well-controlled mechanical loading conditions. In addition, we performed simulations of blood perfusion during tetanic, isometric contraction and maximal vasodilation in a simplified, two-dimensional finite-element model of a rat calf muscle. A vascular waterfall in the venous compartment was identified as the main cause for blood flow impediment both in the experiment and in the finite-element simulations. The validated finite-element model offers possibilities for detailed analysis of blood perfusion in three-dimensional muscle models under complicated loading conditions.