Instantaneous venous return curves in an intact canine preparation

1984 ◽  
Vol 56 (3) ◽  
pp. 765-771 ◽  
Author(s):  
M. R. Pinsky
Keyword(s):  
Venous Return ◽  
Right Atrial ◽  
Negative Slope ◽  
Positive Pressure ◽  
Similar Degree ◽  
Straight Line ◽  
Mean Systemic Pressure ◽  
Relationship Of ◽  
The Relationship ◽  
Stop Flow

The relationship between right atrial pressure (Pra) and venous return describes a venous return curve. Because changes in venous return and right ventricular stroke volume (SVRV) are similar during small tidal volume (VT) breathing, we compared the relationship of SVRV and Pra during positive-pressure ventilation (VT less than 10 ml/kg) in 17 pentobarbital-anesthetized, closed-chest, canine preparations. The SVRV-Pra relationship describes a straight line with a negative slope and a positive mean systemic pressure (Pms)-zero flow intercept (instantaneous Pms). Instantaneous Pms is similar to ventricular fibrillation-induced (stop-flow) Pms (8.1 +/- 0.8 vs. 8.4 +/- 0.7 mmHg, mean +/- SE). With volume infusion, both instantaneous and stop-flow Pms increase to a similar degree (R = 0.9014, P less than 0.001). The effect of opening an arteriovenous fistula is time dependent and variable between dogs, but by 30 s it is associated with an increase in instantaneous Pms (5.2 +/- 3.2 mmHg). Vascular compliance determined by adding and removing blood from the intravascular space displays a curvilinear hysteresis. The instantaneous venous return curve is affected by intravascular blood volume, vasomotor tone, and resistance to venous return. The relationship between SVRV and Pra during small VT breathing define instantaneous venous return curves similar to those described using right-heart bypass preparations.

Dose–response effects of cardiac glycosides on pooling and systemic and pulmonary hemodynamics

1970 ◽  
Vol 48 (8) ◽  
pp. 533-541 ◽  
Author(s):  
Linda T. Archer ◽  
Lerner B. Hinshaw
Keyword(s):  
Cardiac Glycosides ◽  
Venous Return ◽  
Intact Animal ◽  
Peripheral Resistance ◽  
Major Site ◽  
Pulmonary Hemodynamics ◽  
Relationship Of ◽  
The Relationship ◽  
Major Emphasis ◽  
Vascular Region

The effects of ouabain and digoxin on systemic and cardiopulmonary circulations and the degree and site of vascular pooling were evaluated in this study. A major emphasis was placed on the relationship of dosage to responses observed. Experiments were performed on 32 adult mongrel dogs using a venous return (constant cardiac inflow) preparation. Animals were divided into two groups, intact and eviscerated. Mean cumulative doses were 27, 55, and 81 μg/kg for intact ouabain-injected dogs; 21, 42, 63, 84, and 105 μg/kg for intact digoxin-injected dogs; and 26, 52, and 77 μg/kg for eviscerated ouabain-injected dogs. There was a positive correlation between amount of blood pooled and dose of cardiac glycosides given in the intact animal. The statistical difference in pooling at each dose of ouabain between intact and eviscerated animals implicated the hepatosplanchnic vascular bed as a major site of pooling. Since there was a significant statistical increase in total peripheral resistance in intact ouabain-injected dogs but not in ouabain-treated eviscerated animals, the site of peripheral resistance changes appears to be the hepatosplanchnic vascular region. Left atrial pressures rose significantly in intact and eviscerated dogs at higher ouabain doses. These findings underscore the complexity of the mechanisms of action of cardiac glycosides and emphasize the critical importance of dosage, type of glycoside administered, and individual variation of response in the canine species.

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

2002 ◽  
Vol 92 (3) ◽  
pp. 1223-1231 ◽  
Author(s):  
Paul C. M. Van Den Berg ◽  
Jos R. C. Jansen ◽  
Michael R. Pinsky
Keyword(s):  
Cardiac Output ◽  
Venous Return ◽  
Artery Bypass ◽  
Surgical Patients ◽  
Right Atrial ◽  
Bladder Pressure ◽  
Positive Pressure ◽  
Abdominal Pressure ◽  
Heart Rate Data ◽  
End Diastolic Volume

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 cmH2O from 0 to 20 cmH2O in sequential 25-s inspiratory-hold maneuvers. Right ventricular (RV) cardiac output (COtd) and RV ejection fraction (EFrv) were measured at 5 s into the inspiratory-hold maneuver by the thermodilution technique. RV end-diastolic volume and stroke volume were calculated from EFrvand 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 COtdnor RV end-diastolic volume changed. The ratio of change (Δ) in Paw to ΔPra was 0.32 ± 0.20. The ratio of ΔPra to ΔCOtdwas 0.05 ± 00.15 l · min−1· mmHg−1. However, Pabd increased such that the ratio of ΔPra to ΔPabd 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 cmH2O 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.

The relationship of bronchopulmonary dysplasia to the occurrence of alveolar rupture during positive pressure ventilation

1978 ◽  
Vol 6 (3) ◽  
pp. 140-142 ◽  
Author(s):  
FERGUS M. B. MOYLAN ◽  
ALEXANDER M. WALKER ◽  
SANDRA S. KRAMER ◽  
I. DAVID TODRES ◽  
DANIEL C. SHANNON
Keyword(s):  
Bronchopulmonary Dysplasia ◽  
Positive Pressure Ventilation ◽  
Positive Pressure ◽  
Relationship Of ◽  
The Relationship

Cardiovascular effects of positive end-expiratory pressure in dogs

1978 ◽  
Vol 44 (5) ◽  
pp. 743-750 ◽  
Author(s):  
S. S. Cassidy ◽  
C. H. Robertson ◽  
A. K. Pierce ◽  
R. L. Johnson
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Left Atrial ◽  
Cardiovascular Effects ◽  
Esophageal Pressure ◽  
Right Atrial ◽  
Positive Pressure ◽  
Positive End Expiratory Pressure ◽  
Pericardial Pressure ◽  
Relationship Of

Our purpose was to reexamine the relationship of the fall in cardiac output and blood pressure which occurs during positive end-expiratory pressure (PEEP) to changes in transmural right atrial and left atrial filling pressures. Closed-chest dogs, half with pulmonary edema, were studied during spontaneous breathing and inspiratory positive-pressure breathing (IPPB) with 0–15 cmH2O PEEP. Mean esophageal pressure accurately reflected changes in pericardial pressure and was used to estimate extracardiac pressure. We found that cardiac output fell approximately 50% and blood pressure fell 20% during 15 cmH2OPEEP in spite of well maintained transmural right atrial and left atrial (or pulmonary artery wedge) pressures suggesting a primary or reflex depression of atrial or ventricular function.

scholarly journals The Guytonian Equation: Established Physiological Law?

2020 ◽  
Vol 5 (2) ◽  
Author(s):  
George L Brengelmann
Keyword(s):  
Steady State ◽  
Venous Return ◽  
Point Of View ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Peripheral Vasculature ◽  
Systemic Venous Return ◽  
Mean Systemic Pressure ◽  
Zero Flow

The present collection of papers is meant to focus on old and new concepts about venous return. This essay argues that one widely held old concept is wrong. The misconception would be perpetuated by those who speak of “repurposing the systemic venous return model”. The model in question describes systemic venous return as driven through a “resistance to venous return” in proportion to the difference between mean systemic pressure and right atrial pressure. It arose from experiments in which right atrial pressure (Pra) was recorded while flow was forced through the peripheral vasculature by a pump, with data points taken after pressures equilibrated to each new level of flow. The steady-state flow (F) set by the pump could be taken interchangeably as cardiac output (CO) or venous return (VR). Pra at the zero-flow level settled at what is defined as “mean systemic pressure” (Pms), understood as the pressure at which all the elastic segments of the peripheral vasculature equilibrate in the absence of pressure differences associated with flow. Total circulating volume was kept constant, independent of flow level. The data were approximated by the equation Pra = Pms – F*RVR, alternatively written as F = (Pms – Pra)/RVR. From the point of view of the first formulation, we see Pra falling in proportion to F, starting from Pms at zero flow, a concise statement of the actual experimental procedure and findings. The second formulation has been seen from a different perspective; that F is proportional to the net driving pressure, i.e., (Pms – Pra), in which Pra is seen as a back pressure opposing venous return. From this point of view, adopted by a leading researcher of his time, A.C. Guyton, comes the idea that, to increase VR, the heart must somehow reduce Pra. Re-examining the model that Guyton and his coworkers developed reveals that the appearance of Pms in their equation does not identify this variable as a pressure that exists physically at the upstream end of the pathway for venous return. At best, the model offers a way of looking at the factors that determine the equilibrium between the Pra that results in the peripheral vasculature at a particular steady-state level of flow that is consistent with the influence of Pra on the output of the heart. It has nothing to offer for the advancement of understanding of the pathophysiology of real, dynamic flow within vascular segments.

Relationship of venous PO2 to muscle PO2 during hypoxemia

1989 ◽  
Vol 67 (3) ◽  
pp. 1093-1099 ◽  
Author(s):  
G. Gutierrez ◽  
N. Lund ◽  
A. L. Acero ◽  
C. Marini
Keyword(s):  
Vena Cava ◽  
Biceps Femoris ◽  
Right Atrial ◽  
Tissue Cell ◽  
Mechanically Ventilated ◽  
Biceps Femoris Muscle ◽  
Post Hoc ◽  
Relationship Of ◽  
The Relationship ◽  
Arterial Po2

Anesthetized mechanically ventilated rabbits were subjected to progressive hypoxemia (n = 7) to determine the relationship of venous PO2 (PvO2) to skeletal muscle PO2 (PtiO2). Measures of arterial PO2 (PaO2), right atrial PO2 [(PvO2)RA], and hindlimb PO2 [(PvO2)limb], were obtained from the carotid artery, right atrium, and inferior vena cava, just above the level of the iliac bifurcation. Biceps femoris muscle PtiO2 was measured with a surface O2 microelectrode having eight measuring points. PaO2 was decreased from 90.3 +/- 5.4 to 26.8 +/- 0.8 Torr in five consecutive steps, followed by reoxygenation to 105.6 +/- 10.5 (SE) Torr. Measurements were obtained after each decrement in PaO2. A total of 128 measures of PtiO2 were obtained per experimental stage. The mean and distribution of the muscle PtiO2 histogram were determined. Measurements were compared with analysis of variance and the Newman-Keuls post hoc method. (PvO2)limb had similar values as the average muscle PtiO2 (PtiO2) for PaO2 values greater than 52.1 +/- 4.3 Torr, where (PvO2)limb became greater than PtiO2 (P less than 0.05). The lowest measures of (PvO2)limb and PtiO2 were 15.9 +/- 0.7 and 4.0 +/- 0.1 Torr, respectively (P less than 0.01). The PtiO2 histograms showed no evidence of increased microvascular heterogeneity with hypoxemia. We conclude that in hypoxemia PvO2 is greater than muscle PtiO2. This difference may be related to the establishment of significant physicochemical O2 gradients from erythrocyte to tissue cell.

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

2003 ◽  
Vol 94 (3) ◽  
pp. 849-859 ◽  
Author(s):  
George L. Brengelmann
Keyword(s):  
Critical Analysis ◽  
Venous Return ◽  
Back Pressure ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Input Output ◽  
The One ◽  
Mean Systemic Pressure

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.

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