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Venous return and mean systemic filling pressure: physiology and clinical applications.

ABSTRACT: Venous return is the flow of blood from the systemic venous network towards the right heart. At steady state, venous return equals cardiac output, as the venous and arterial systems operate in series. However, unlike the arterial one, the venous network is a capacitive system with a high compliance. It includes a part of unstressed blood, which is a reservoir that can be recruited via sympathetic endogenous or exogenous stimulation. Guyton's model describes the three determinants of venous return: the mean systemic filling pressure, the right atrial pressure and the resistance to venous return. Recently, new methods have been developed to explore such determinants at the bedside. In this narrative review, after a reminder about Guyton's model and current methods used to investigate it, we emphasize how Guyton's physiology helps understand the effects on cardiac output of common treatments used in critically ill patients.

SUBMITTER: Persichini R

PROVIDER: S-EPMC9128096 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature

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Venous return and mean systemic filling pressure: physiology and clinical applications.

Persichini Romain R Lai Christopher C Teboul Jean-Louis JL Adda Imane I Guérin Laurent L Monnet Xavier X

Critical care (London, England) 20220524 1

Venous return is the flow of blood from the systemic venous network towards the right heart. At steady state, venous return equals cardiac output, as the venous and arterial systems operate in series. However, unlike the arterial one, the venous network is a capacitive system with a high compliance. It includes a part of unstressed blood, which is a reservoir that can be recruited via sympathetic endogenous or exogenous stimulation. Guyton's model describes the three determinants of venous retur ...[more]

PMID: 35610620

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Project description:Mean systemic filling pressure (Pms) is a promising parameter in determining intravascular fluid status. Pms derived from venous return curves during inspiratory holds with incremental airway pressures (Pms-Insp) estimates Pms reliably but is labor-intensive. A computerized algorithm to calculate Pms (Pmsa) at the bedside has been proposed. In previous studies Pmsa and Pms-Insp correlated well but with considerable bias. This observational study was performed to validate Pmsa with Pms-Insp in cardiac surgery patients. Cardiac output, right atrial pressure and mean arterial pressure were prospectively recorded to calculate Pmsa using a bedside monitor. Pms-Insp was calculated offline after performing inspiratory holds. Intraclass-correlation coefficient (ICC) and assessment of agreement were used to compare Pmsa with Pms-Insp. Bias, coefficient of variance (COV), precision and limits of agreement (LOA) were calculated. Proportional bias was assessed with linear regression. A high degree of inter-method reliability was found between Pmsa and Pms-Insp (ICC 0.89; 95%CI 0.72-0.96, p = 0.01) in 18 patients. Pmsa and Pms-Insp differed not significantly (11.9 mmHg, IQR 9.8-13.4 vs. 12.7 mmHg, IQR 10.5-14.4, p = 0.38). Bias was -0.502 ± 1.90 mmHg (p = 0.277). COV was 4% with LOA -4.22 - 3.22 mmHg without proportional bias. Conversion coefficient Pmsa ➔ Pms-Insp was 0.94. This assessment of agreement demonstrates that the measures Pms-Insp and the computerized Pmsa-algorithm are interchangeable (bias -0.502 ± 1.90 mmHg with conversion coefficient 0.94). The choice of Pmsa is straightforward, it is non-interventional and available continuously at the bedside in contrast to Pms-Insp which is interventional and calculated off-line. Further studies should be performed to determine the place of Pmsa in the circulatory management of critically ill patients. ( www.clinicaltrials.gov ; TRN NCT04202432, release date 16-12-2019; retrospectively registered).Clinical Trial Registration www.ClinicalTrials.gov , TRN: NCT04202432, initial release date 16-12-2019 (retrospectively registered).

Project description:Background: A decade ago, it became possible to derive mean systemic filling pressure (MSFP) at the bedside using the inspiratory hold maneuver. MSFP has the potential to help guide hemodynamic care, but the estimation is not yet implemented in common clinical practice. In this study, we assessed the ability of MSFP, vascular compliance (Csys), and stressed volume (Vs) to track fluid boluses. Second, we assessed the feasibility of implementation of MSFP in the intensive care unit (ICU). Exploratory, a potential difference in MSFP response between colloids and crystalloids was assessed. Methods: This was a prospective cohort study in adult patients admitted to the ICU after cardiac surgery. The MSFP was determined using 3-4 inspiratory holds with incremental pressures (maximum 35 cm H2O) to construct a venous return curve. Two fluid boluses were administered: 100 and 500 ml, enabling to calculate Vs and Csys. Patients were randomized to crystalloid or colloid fluid administration. Trained ICU consultants acted as study supervisors, and protocol deviations were recorded. Results: A total of 20 patients completed the trial. MSFP was able to track the 500 ml bolus (p < 0.001). In 16 patients (80%), Vs and Csys could be determined. Vs had a median of 2029 ml (IQR 1605-3164), and Csys had a median of 73 ml mmHg-1 (IQR 56-133). A difference in response between crystalloids and colloids was present for the 100 ml fluid bolus (p = 0.019) and in a post hoc analysis, also for the 500 ml bolus (p = 0.010). Conclusion: MSFP can be measured at the bedside and provides insights into the hemodynamic status of a patient that are currently missing. The clinical feasibility of Vs and Csys was judged ambiguously based on the lack of required hemodynamic stability. Future studies should address the clinical obstacles found in this study, and less-invasive alternatives to determine MSFP should be further explored. Clinical Trial Registration: ClinicalTrials.gov Identifier NCT03139929.

Project description:BackgroundMean circulatory filling pressure (Pmcf) provides information on stressed volume and is crucial for maintaining venous return. This study investigated the Pmcf and other determinants of venous return in dysrhythmic and asphyxial circulatory shock and arrest.MethodsTwenty Landrace/Large-White piglets were allocated into two groups of 10 animals each. In the dysrhythmic group, ventricular fibrillation was induced with a 9 V cadmium battery, while in the asphyxia group, cardiac arrest was induced by stopping and disconnecting the ventilator and clamping the tracheal tube at the end of exhalation. Mean circulatory filling pressure was calculated using the equilibrium mean right atrial pressure at 5-7.5 s after the onset of cardiac arrest and then every 10 s until 1 min post-arrest. Successful resuscitation was defined as return of spontaneous circulation (ROSC) with a MAP of at least 60 mmHg for a minimum of 5 min.ResultsAfter the onset of asphyxia, a ΔPmca increase of 0.004 mmHg, 0.01 mmHg, and 1.26 mmHg was observed for each mmHg decrease in PaO2, each mmHg increase in PaCO2, and each unit decrease in pH, respectively. Mean Pmcf value in the ventricular fibrillation and asphyxia group was 14.81 ± 0.5 mmHg and 16.04 ± 0.6 mmHg (p < 0.001) and decreased by 0.031 mmHg and 0.013 mmHg (p < 0.001), respectively, for every additional second passing after the onset of cardiac arrest. With the exception of the 5-7.5 s time interval, post-cardiac arrest right atrial pressure was significantly higher in the asphyxia group. Mean circulatory filling pressure at 5 to 7.5 s after cardiac arrest predicted ROSC in both groups, with a cut-off value of 16 mmHg (AUC = 0.905, p < 0.001).ConclusionMean circulatory filling pressure was higher in hypoxic hypercapnic conditions and decreased at a lower rate after cardiac arrest compared to normoxemic and normocapnic state. A Pmcf cut-off point of 16 mmHg at 5-7.5 s after cardiac arrest can highly predict ROSC.

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Venous return and mean systemic filling pressure: physiology and clinical applications.

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Venous return and mean systemic filling pressure: physiology and clinical applications.

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