Effect of negative intrathoracic pressure on venous return

In acute experiments on cats and in observations made in human subjects, an increase of the negative intrathoracic pressure (NIP) leads to no significant changes of the venous return (VR) mean values. The peak values of the VR, however, increased and decreased more in inspiration and expiration following a deep breathing as compared with the normal breathing. The NIP seems to exert no direct effect upon the VR.     

Effects of augmented respiratory muscle pressure production on locomotor limb venous return during calf contraction exercise.

We determined effects of augmented inspiratory and expiratory intrathoracic pressure or abdominal pressure (Pab) excursions on within-breath changes in steady-state femoral venous blood flow (Qfv) and net Qfv during tightly controlled (total breath time = 4 s, duty cycle = 0.5) accessory muscle/"rib cage" (DeltaPab <2 cmH2O) or diaphragmatic (DeltaPab >5 cmH2O) breathing. Selectively augmenting inspiratory intrathoracic pressure excursion during rib cage breathing augmented inspiratory facilitation of Qfv from the resting limb (69% and 89% of all flow occurred during nonloaded and loaded inspiration, respectively); however, net Qfv in the steady state was not altered because of slight reductions in femoral venous return during the ensuing expiratory phase of the breath. Selectively augmenting inspiratory esophageal pressure excursion during a predominantly diaphragmatic breath at rest did not alter within-breath changes in Qfv relative to nonloaded conditions (net retrograde flow = -9 +/- 12% and -4 +/- 9% during nonloaded and loaded inspiration, respectively), supporting the notion that the inferior vena cava is completely collapsed by relatively small increases in gastric pressure. Addition of inspiratory + expiratory loading to diaphragmatic breathing at rest resulted in reversal of within-breath changes in Qfv, such that >90% of all anterograde Qfv occurred during inspiration. Inspiratory + expiratory loading also reduced steady-state Qfv during mild- and moderate-intensity calf contractions compared with inspiratory loading alone. We conclude that 1) exaggerated inspiratory pressure excursions may augment within-breath changes in femoral venous return but do not increase net Qfv in the steady state and 2) active expiration during diaphragmatic breathing reduces the steady-state hyperemic response to dynamic exercise by mechanically impeding venous return from the locomotor limb, which may contribute to exercise limitation in health and disease.     

Influence of positive airway pressure on the pressure gradient for venous return in humans.

To study the effect of positive airway pressure (Paw) on the pressure gradient for venous return [the difference between mean systemic filling pressure (Pms) and right atrial pressure (Pra)], we investigated 10 patients during general anesthesia for implantation of defibrillator devices. Paw was varied under apnea from 0 to 15 cmH(2)O, which increased Pra from 7.3 +/- 3.1 to 10.0 +/- 2.3 mmHg and decreased left ventricular stroke volume by 23 +/- 22%. Episodes of ventricular fibrillation, induced for defibrillator testing, were performed during 0- and 15-cmH(2)O Paw to measure Pms (value of Pra 7.5 s after onset of circulatory arrest). Positive Paw increased Pms from 10.2 +/- 3.5 to 12.7 +/- 3.2 mmHg, and thus the pressure gradient for venous return (Pms - Pra) remained unchanged. Echocardiography did not reveal signs of vascular collapse of the inferior and superior vena cava due to lung expansion. In conclusion, we demonstrated that positive Paw equally increases Pra and Pms in humans and alters venous return without changes in the pressure gradient (Pms - Pra).     

Effect of positive pressure on venous return in volume-loaded cardiac surgical patients.

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.     

Effects of inspiratory diaphragmatic descent on inferior vena caval venous return.

To explain the contradictory results in the literature regarding the effects of inspiratory diaphragmatic descent on inferior vena caval (IVC) venous return, we evaluated changes in total IVC flow as well as regional splanchnic and nonsplanchnic IVC flows by use of ultrasound flow probes placed around the thoracic and subhepatic abdominal IVC during phrenic nerve stimulation (PNS) in anesthetized open-chest dogs. With the abdomen closed (n = 6), PNS under hypervolemic conditions increased the total IVC flow by enhancing the splanchnic IVC flow, with a transient decrease in the nonsplanchnic IVC flow (P less than 0.05). Under hypovolemic conditions, PNS initially increased the total IVC flow but later decreased the total IVC flow by reducing the nonsplanchnic IVC flow, associated with a venous pressure gradient in the IVC across the diaphragm (P less than 0.05), consistent with development of a vascular waterfall. With the abdomen widely open, the mobile abdominal contents eviscerated, and the subhepatic IVC occluded (n = 5), PNS increased the splanchnic IVC flow associated only with an increase in focal contact pressure over the liver without any increase in general abdominal pressure (Pab) (P less than 0.05). These results suggest that our previously proposed concept of abdominal vascular zone conditions (J. Appl. Physiol. 69: 1961-1972, 1990) is useful as a global approximation to understand the effects of respiratory-induced changes in Pab's on the total and regional IVC venous return. Nonhomogeneous distribution of Pab's during diaphragmatic descent may need to be considered to explain all aspects of the behavior of the intact IVC system.     

Correction of venous congestion in abdominal organs under antiorthostatic conditions

The effect of a diuretic on the ultrasound pattern of venous congestion in abdominal organs in a healthy subject staying in an antiorthostatic position (AOP, 15°) for 12 h was studied. After furosemide administration, the circulating plasma volume (CPV), total water content of the body, and extracellular fluid volume decreased more than without the treatment. Overall hypohydration of the body prevented the dilation of hepatic veins typical of an AOP while not affecting noticeably the venous congestion in the portal vein system. In addition, the administration of the diuretic prevented the activation of bile secretion and an increased gastric juice secretion under antiorthostatic conditions. Thus, it was demonstrated that pharmacological hypohydration, by decreasing the CPV and the blood pressure in the inferior vena cava, unloads hepatic veins and prevents enhanced secretion in organs of the digestive system under the conditions of gravitational redistribution of body fluids.     

Left ventricular reflex control of venous return and systemic vascular capacitance in dogs

The reflex effects of left ventricular distension on venous return, vascular capacitance, vascular resistance, and sympathetic efferent nerve activity were examined in dogs anesthetized with sodium pentobarbital. In addition, the interaction of left ventricular distension and the carotid sinus baroreflex was examined. Vascular capacitance was assessed by measuring changes in systemic blood volume, using extracorporeal circulation with constant cardiac output and constant central venous pressure. Left ventricular distension produced by balloon inflation caused a transient biphasic change in venous return; an initial small increase was followed by a late relatively large decrease. Left ventricular distension increased systemic blood volume by 3.8 +/- 0.6 mL/kg and decreased systemic blood pressure by 27 +/- 2 mmHg (1 mmHg = 133.3 Pa) at an isolated carotid sinus pressure of 50 mmHg. These changes were accompanied by a simultaneous decrease in sympathetic efferent nerve activity. When the carotid sinus pressure was increased to 125 and 200 mmHg, these responses were attenuated. It is suggested that left ventricular mechanoreceptors and carotid baroreceptors contribute importantly to the control of venous return and vascular capacitance.     

Effects of pleural pressure and abdominal pressure on diaphragmatic blood flow

Alveolar transfer of prostaglandin E2 (PGE2) was characterized in isolated perfused guinea pig lungs (n = 19) by measuring radioactivity appearing in the venous effluent during 30 min after intratracheal instillation of [3H]PGE2, [14C]-mannitol, and [125I]iodoantipyrine. Recovery of lipid-soluble [125I]iodoantipyrine [91 +/- 3% (SE)] after 30 min was used to estimate total 3H and 14C delivered to the exchanging region of lung at time 0. In seven control lungs, 58 +/- 4% of [14C]mannitol and 16 +/- 4% of [3H]PGE2 was retained 10 min after instillation. Neither perfusion with diphloretin phosphate (10 micrograms/ml; n = 4) nor hypothermia (5 degrees C; n = 5) significantly affected the amount of [14C]mannitol retained; however, [3H]PGE2 remaining in these lungs increased significantly to 36 +/- 4 and 53 +/- 2%, respectively. Addition of unlabeled PGE2 (200 micrograms) to the instilled solution (n = 3) increased retention of both [14C]mannitol (80 +/- 3%) and [3H]PGE2 (65 +/- 4%). Alveolar transfer of [3H]PGE2 was calculated as the difference in percent retention of [14C]mannitol and [3H]PGE2 and normalized to that of [14C]mannitol. After 10 min, alveolar transfer of [3H]PGE2 was 71 +/- 8% in control lungs but was decreased to 26 +/- 7, 10 +/- 5, and 19 +/- 6% by diphloretin phosphate, hypothermia, or unlabeled PGE2, respectively. These data suggest that alveolar clearance of PGE2 involves a saturable drug- and temperature-sensitive process.     

Dynamic components of interrelation among the parameters of heart preload, venous return and central venous pressure

In acute experiments on cats, in applying of original methodical approach--control of systemic circulation by the aid of computerized negative feedback loop changing the volume of circulating blood (method of biological feedback)--first were experimentally measured and analyzed the dynamic characteristics of relationship between central venous pressure and venous return of blood to the right heart. The following positions are offered and validated in the work. (1) It is shown that the passive component (mechanical compliance) is more important than active one (active myogenic component) in the small circle of circulation being compared to large one. (2) Venous return plays the leading role in forming the shifts of central venous pressure directly during developing of the transition processes of systemic circulation caused by the norepinephrine injection and the linear type of this link is proved directly during the development of the cardiovascular shift. (3) The dynamic characteristics of relationship between venous return and central venous pressure during the geodynamical reaction caused by the shifts of intravascular blood volume are experimentally measured and mathematically analyzed. It is revealed that dynamic summands of this link may overbalance the static ones known before in influence on the total shifts in developing of the systemic reaction of circulation and this influence increases when the velocity of changes in studied parameters of circulation becomes more.     

Effects of autonomic disruption and inactivity on venous vascular function

The effects of autonomic disruption and inactivity were studied on the venous vascular system. Forty-eight subjects, 24 with spinal cord injury (SCI) and 12 sedentary and 12 active able-bodied controls, participated in this study. Peripheral autonomic data were obtained to estimate sympathetic vasomotor control [low-frequency component of systolic blood pressure (LF(SBP))]. Vascular parameters were determined using strain-gauge venous occlusion plethysmography: venous capacitance (VC), venous emptying rate (VER), and total venous outflow (VO(t)). An additional vascular parameter was calculated: venous compliance [(VC/occlusion pressure) x 100]. VC and VO(t) were significantly different (SCI < sedentary < active). VER adjusted for VC was not different for any group comparison, whereas venous compliance was significantly lower in the SCI group than in the able-bodied groups and in the sedentary group compared with the active group. Regression analysis for the total group revealed a significant relationship between LF(SBP) and venous compliance (r = 0.64, P < 0.0001). After controlling for LF(SBP) through analysis of covariance, we found that mean differences for all venous vascular parameters did not change from unadjusted mean values. Our findings suggest that in subjects with SCI, the loss of sympathetic vasomotor tone contributes more than inactivity to reductions in venous vascular function. Heightened VC, VO(t), vasomotor tone, and venous compliance in the active group compared with the sedentary group imply that regular endurance training contributes to optimal venous vascular function and peripheral autonomic integrity.     

A critical analysis of the view that right atrial pressure determines venous return.

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 right atrial pressure (Pra) and flow simultaneously consistent with independent properties of the heart and vasculature. He showed how this point would change with altered properties of the heart (e.g., contractility, sensitivity to preload) and/or of the vasculature (e.g., resistance, total volume). In such graphical representations of negative feedback between two subdivisions of a system, one input/output relationship is necessarily plotted backward, i.e., with the input variable on the y-axis (here, the venous return curve). Unfortunately, this format encourages mistaken ideas about the role of Pra as a "back pressure," such as the assertion that elevating Pra to the level of mean systemic pressure would stop venous return. These concepts are reexamined through review of the original experiments on venous return, presentation of a hypothetical alternative way for obtaining the same data, and analysis of a simple model.     

Influence of extravascular pressure on changes induced in vascular resistance in the small intestine by elevated venous pressure

The influence of the extravascular pressure on the size of the increase in vascular resistance after elevation of venous outflow pressure (venous-vasomotor response) was studied in an intestinal segment, perfused at a constant rate, in anaesthetized dogs. If pressure in the lumen of the intestine was elevated (spontaneously, pharmacologically, mechanically) or pressure in the plethysmograph was raised, venous-vasomotor responses were either smaller or absent. When pressure in the intestinal lumen was raised, blood volume increments produced in the segment by elevated venous pressure were significantly smaller than those observed in the presence of resting pressure. The presence of a venous-vasomotor response was correlated to the quantitative relationship between the extravascular and the venous pressure. Its induction was dependent on whether the outflow venous pressure was higher than the pressure values in the intestinal lumen or the plethysmograph; in that case it developed to an extent corresponding to the increment in transmural vascular pressure.     

Intravascular pressure profiles in elephant seals: hypotheses on the caval sphincter, extradural vein and venous return to the heart

In order to evaluate hemodynamics in the complex vascular system of phocid seals, intravascular pressure profiles were measured during periods of rest-associated apnea in young elephant seals (Mirounga angustirostris). There were no significant differences between apneic and eupneic mean arterial pressures. During apnea, venous pressure profiles (pulmonary artery, thoracic portion of the vena cava (thoracic vena cava), extradural vein, and hepatic sinus) demonstrated only minor, transient fluctuations. During eupnea, all venous pressure profiles were dominated by respiratory fluctuations. During inspiration, pressures in the thoracic vena cava and extradural vein decreased -9 to -21 mm Hg, and -9 to -17 mm Hg, respectively. In contrast, hepatic sinus pressure increased 2-6 mm Hg during inspiration. Nearly constant hepatic sinus and intrathoracic vascular pressure profiles during the breath-hold period are consistent with incomplete constriction of the caval sphincter during these rest-associated apneas. During eupnea, negative inspiratory intravascular pressures in the chest ("the respiratory pump") should augment venous return via both the venae cavae and the extradural vein. It is hypothesized that, in addition to the venae cavae, the prominent para-caval venous system of phocid seals (i.e., the extradural vein) is necessary to allow adequate venous return for maintenance of high cardiac outputs and blood pressure during eupnea.     

Effects of parabolic flight on abdominal arterial pressure in conscious rats.

Abdominal arterial pressure during parabolic flight was measured using a telemetry system to clarify the acute effect of microgravity on hemodynamics in conscious rats. The microgravity condition was elicited by three different levels of entry gravity, i.e. 2 G, 1.5 G and 1 G. On exposure to 2 G, mean aortic pressure (MBP) increased up to 118.7 mm Hg +/- 7.3 compared with the value at 1 G (107.0 +/- 6.3 mm Hg, n=6). The value at microgravity preceded by 2 G was 118.0 mmHg +/- 5.2 mm HG and it was still higher than at 1 G. When 1.5 G was elicited before microgravity exposure, MBP also increased (1.5 G: 114.9 +/- 5.3 vs 1 G: 105.8+/-5.0 mm Hg) and the value at microgravity was 117.3 + /- 5.3 mmHg. During pre-microgravity maneuver with 1 G, no changes were observed compared with the control level at 1 G (pre-microgravity: 105.0 +/- 5.0 vs 1G: 104.8 +/- 5.1 mm Hg ), whereas the MBP increased up to 117.0 +/- 6.5 mm Hg on exposure to microgravity. From these results, we found that in conscious rat MBP increase during acute microgravity exposure with either 1 G or hyper-G entry.     

Effects of positive end-expiratory pressure ventilation on cerebral venous pressure with head elevation in dogs.

Mechanical ventilation with positive end-expiratory pressure (PEEP) may prevent venous air embolism in the sitting position because cerebral venous pressure (Pcev) could be increased by the PEEP-induced increase in right atrial pressure (Pra). Whereas it is clear that there is a linear transmission of the PEEP-induced increase in Pra to Pcev while the dog is in the prone position, the mechanism of the transmission with the dog in the head-elevated position is unclear. We tested the hypothesis that a Starling resistor-type mechanism exists in the jugular veins when the head is elevated. In one group of dogs, increasing PEEP linearly increased Pcev with the dog in the prone position (head at heart level, slope = 0.851) but did not increase Pcev when the head was elevated. In another group of dogs, an external chest binder was used to produce a larger PEEP-induced increase in Pra. Further increasing Pra increased Pcev only after Pra exceeded a pressure of 19 mmHg (break pressure). This sharp inflection in the upstream (Pcev)-downstream (Pra) relationship suggests that this may be caused by a Starling resistor-type mechanism. We conclude that jugular venous collapse serves as a significant resistance in the transmission of Pra to Pcev in the head-elevated position.